Advances in the Immunobiology of Parasitic Diseases

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 41282

Special Issue Editors


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Guest Editor
Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla 54090, Mexico
Interests: immunoregulation in parasitic diseases; helminths; dendritic cell; macrophage’s response to inflammatory stimulus; interactions between helminths and their molecules with the host; inflammatory-mediated diseases
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Guest Editor
Department of Immunology, Universidad Nacional Autonóma de México, México City 04510, México
Interests: gender differences in host-parasite interactions; sex-associated susceptibility to parasitic diseases as well as environmental pollution and its impact on parasitic diseases
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Physiology and Pharmacology, University of Calgary, AB T2N 4N1, Canada
Interests: To advance knowledge on the regulation of intestinal epithelial biology; mucosal immunology (particularly macrophages) and to assess host-parasite interactions as a way to unravel new approaches to inflammatory disease

Special Issue Information

Dear Colleagues,

Notwithstanding that today, most biomedical research is focused on the pandemic caused by the virus SARs-CoV-2, we still have in the world many diseases unresolved that are now almost forgotten. Thus, when this virus is finally under control, the other diseases caused by different pathogens will remain, causing the same health problems and even worse, due to inattention in the last one and a half year or maybe more.

Parasitic diseases have been deeply rooted in human evolution and will prevail for many years to come. Thus, it is critical that do not forget about the damage they cause to the people who are suffering from these infections. The only way to eradicate or control such parasitic diseases is to increase our knowledge on them.

Therefore, the goal of this Special Issue is to put together the recent findings achieved, despite the pandemic, by researchers interested in parasitic diseases.

This Special Issue invites either original research or review articles focused on, but not limited to, the following “hot topics” in parasitic research:

  • Immunomodulation on parasitic diseases, including protozoa and helminths;
  • Innate immunity to protozoa and helminths;
  • Cytokines/chemokines and susceptibility or resistance on parasitic diseases;
  • Co-infections;
  • Co-morbidities during parasitic infections, for good or bad?
  • Signaling pathways and susceptibility to parasites;
  • Vaccine development against parasites.

Dr. Luis I. Terrazas
Dr. Jorge Morales-Montor
Dr. Derek M. McKay
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • protozoa
  • helminths
  • cytokines
  • signaling pathways
  • co-infections
  • infections and co-morbidities
  • innate immunity
  • immunomodulation
  • immune checkpoints
  • vaccines

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Published Papers (12 papers)

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Editorial

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5 pages, 208 KiB  
Editorial
Advances in the Immunobiology of Parasitic Diseases
by Jorge Morales-Montor, Derek M. McKay and Luis I. Terrazas
Pathogens 2022, 11(7), 811; https://doi.org/10.3390/pathogens11070811 - 20 Jul 2022
Viewed by 1725
Abstract
Notwithstanding that most biomedical research today focuses on the pandemic caused by the SARs-CoV-2 virus, there are many unresolved diseases that are almost forgotten worldwide [...] Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)

Research

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13 pages, 6049 KiB  
Article
Mast-Cell Response to Leishmania mexicana and Sand-Fly Salivary Proteins Is Modulated by Orchiectomy
by Laura Sánchez-García, Armando Pérez-Torres, Samira Muñoz-Cruz, Norma Salaiza-Suazo, Jorge Morales-Montor and Ingeborg Becker
Pathogens 2022, 11(4), 398; https://doi.org/10.3390/pathogens11040398 - 25 Mar 2022
Cited by 2 | Viewed by 2682
Abstract
Mast cells (MCs) play a crucial role during Leishmania infections, which is transmitted through the bite of an infected sand fly that injects saliva together with the parasite. Sand fly saliva is a complex fluid that modulates the host immune response. In addition, [...] Read more.
Mast cells (MCs) play a crucial role during Leishmania infections, which is transmitted through the bite of an infected sand fly that injects saliva together with the parasite. Sand fly saliva is a complex fluid that modulates the host immune response. In addition, hormonal factors modulate the host immune response and alter susceptibility to infections. Thus, to assess the impact of male sex hormones on the mast-cell (MC) response to Leishmania infections, we orchiectomized male mice, infected them with the parasite in the presence of sand fly salivary proteins, and analyzed the inflammatory response of MCs. Our results showed that the MC response to the parasite and vector salivary proteins differed between orchiectomized and sham-operated mice. In orchiectomized mice, MC showed a retarded activation pattern, associated with slower degranulation and weaker TNF-α, histamine, and tryptase staining in response to the infection with Leishmania mexicana combined with vector-salivary proteins, as compared to sham mice. Furthermore, neutrophil infiltration was slower in orchiectomized mice, and numbers of infected macrophages and lesion sizes were smaller. Our results show that, during Leishmania infection, male sex hormones modulate the mast-cell response against the parasite and salivary proteins of the sand fly vector, inducing an intense inflammatory response. Their absence in orchiectomized mice retards the inflammatory response, enabling better control of the infection and slower disease progression. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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15 pages, 1472 KiB  
Article
Sexual Dimorphism of the Neuroimmunoendocrine Response in the Spleen during a Helminth Infection: A New Role for an Old Player?
by Karen Elizabeth Nava-Castro, Lenin Pavón, Luis Enrique Becerril-Villanueva, María Dolores Ponce-Regalado, Hugo Aguilar-Díaz, Mariana Segovia-Mendoza and Jorge Morales-Montor
Pathogens 2022, 11(3), 308; https://doi.org/10.3390/pathogens11030308 - 1 Mar 2022
Cited by 3 | Viewed by 2376
Abstract
The interaction of the nervous, immune, and endocrine systems is crucial in maintaining homeostasis in vertebrates, and vital in mammals. The spleen is a key organ that regulates the neuroimmunoendocrine system. The Taenia crassiceps mouse system is an excellent experimental model to study [...] Read more.
The interaction of the nervous, immune, and endocrine systems is crucial in maintaining homeostasis in vertebrates, and vital in mammals. The spleen is a key organ that regulates the neuroimmunoendocrine system. The Taenia crassiceps mouse system is an excellent experimental model to study the complex host–parasite relationship, particularly sex-associated susceptibility to infection. The present study aimed to determine the changes in neurotransmitters, cytokines, sex steroids, and sex-steroid receptors in the spleen of cysticercus-infected male and female mice and whole parasite counts. We found that parasite load was higher in females in comparison to male mice. The levels of the neurotransmitter epinephrine were significantly decreased in infected male animals. The expression of IL-2 and IL-4 in the spleen was markedly increased in infected mice; however, the expression of Interleukin (IL)-10 and interferon (IFN)-γ decreased. We also observed sex-associated differences between non-infected and infected mice. Interestingly, the data show that estradiol levels increased in infected males but decreased in females. Our studies provide evidence that infection leads to changes in neuroimmunoendocrine molecules in the spleen, and these changes are dimorphic and impact the establishment, growth, and reproduction of T. crassiceps. Our findings support the critical role of the neuroimmunoendocrine network in determining sex-associated susceptibility to the helminth parasite. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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17 pages, 2676 KiB  
Article
Characterisation of Macrophage Polarisation in Mice Infected with Ninoa Strain of Trypanosoma cruzi
by Dunia M. Medina-Buelvas, Miriam Rodríguez-Sosa and Libia Vega
Pathogens 2021, 10(11), 1444; https://doi.org/10.3390/pathogens10111444 - 6 Nov 2021
Cited by 5 | Viewed by 2472
Abstract
Macrophages (MΦ) play a key role in the development of the protective immune response against Trypanosoma cruzi infection. To determine the role of MΦ subtypes M1 and M2 in the development of immunity against the Mexican strain of T. cruzi (Ninoa strain), we [...] Read more.
Macrophages (MΦ) play a key role in the development of the protective immune response against Trypanosoma cruzi infection. To determine the role of MΦ subtypes M1 and M2 in the development of immunity against the Mexican strain of T. cruzi (Ninoa strain), we have analysed in a time course the infection and characterised the M1 and M2 subtypes in two mouse models, BALB/c and C57BL/6. After infection, BALB/c mice developed an increased blood parasite load and the parasites were cleared from the blood one week later than in C57BL/6 mice. However, similar cellular infiltrate and cardiac alterations were observed between BALB/c and C57BL/6 mice. At 36 days, the T. cruzi infection differentially modulated the expression of immune cells, and both the BALB/c and C57BL/6 mice significantly reduced TCD4+ cells. However, BALB/c mice produced significantly more TCD8+ than C57BL/6 mice in the spleen and lymph nodes. Furthermore, BALB/c mice produce significantly more MΦ in the spleen, while C57BL/6 produce similar levels to uninfected mice. The M1 MΦ ratio increased significantly at 3–5 days post-infection (dpi), but then decreased slightly. On the contrary, the M2 MΦ were low at the beginning of the infection, but the proportion of M1 and M2 MΦ at 36 dpi was similar. Importantly, the MΦ subtypes M2c and M2d significantly increased the induction of tissue repair by the end of the acute phase of the infection. These results indicate that the Ninoa strain has developed strategies to modulate the immune response, with fine differences depending on the genetic background of the host. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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16 pages, 21330 KiB  
Article
STAT1-Dependent Recruitment of Ly6ChiCCR2+ Inflammatory Monocytes and M2 Macrophages in a Helminth Infection
by Mireya Becerra-Díaz, Yadira Ledesma-Soto, Jonadab E. Olguín, Angel Sánchez-Barrera, Mónica G. Mendoza-Rodríguez, Sandy Reyes, Abhay R. Satoskar and Luis I. Terrazas
Pathogens 2021, 10(10), 1287; https://doi.org/10.3390/pathogens10101287 - 6 Oct 2021
Cited by 4 | Viewed by 2806
Abstract
Signal Transducer and Activator of Transcription (STAT) 1 signaling is critical for IFN-γ-mediated immune responses and resistance to protozoan and viral infections. However, its role in immunoregulation during helminth parasitic infections is not fully understood. Here, we used STAT1−/− mice to investigate [...] Read more.
Signal Transducer and Activator of Transcription (STAT) 1 signaling is critical for IFN-γ-mediated immune responses and resistance to protozoan and viral infections. However, its role in immunoregulation during helminth parasitic infections is not fully understood. Here, we used STAT1−/− mice to investigate the role of this transcription factor during a helminth infection caused by the cestode Taenia crassiceps and show that STAT1 is a central molecule favoring susceptibility to this infection. STAT1−/− mice displayed lower parasite burdens at 8 weeks post-infection compared to STAT1+/+ mice. STAT1 mediated the recruitment of inflammatory monocytes and the development of alternatively activated macrophages (M2) at the site of infection. The absence of STAT1 prevented the recruitment of CD11b+Ly6ChiLy6G monocytic cells and therefore their suppressive activity. This failure was associated with the defective expression of CCR2 on CD11b+Ly6ChiLy6G cells. Importantly, CD11b+Ly6ChiLy6G cells highly expressed PDL-1 and suppressed T-cell proliferation elicited by anti-CD3 stimulation. PDL-1+ cells were mostly absent in STAT1−/− mice. Furthermore, only STAT1+/+ mice developed M2 macrophages at 8 weeks post-infection, although macrophages from both T. crassiceps-infected STAT1+/+ and STAT1−/− mice responded to IL-4 in vitro, and both groups of mice were able to produce the Th2 cytokine IL-13. This suggests that CD11b+CCR2+Ly6ChiLy6G cells give rise to M2 macrophages in this infection. In summary, a lack of STAT1 resulted in impaired recruitment of CD11b+CCR2+Ly6ChiLy6G cells, failure to develop M2 macrophages, and increased resistance against T. crassiceps infection. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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12 pages, 2878 KiB  
Article
An Exaggerated Immune Response in Female BALB/c Mice Controls Initial Toxoplasma gondii Multiplication but Increases Mortality and Morbidity Relative to Male Mice
by Rasha Alonaizan, Stuart Woods, Kerrie E Hargrave and Craig W. Roberts
Pathogens 2021, 10(9), 1154; https://doi.org/10.3390/pathogens10091154 - 8 Sep 2021
Cited by 6 | Viewed by 2416
Abstract
Studies indicate that female mice are more susceptible to T. gondii infection, as defined by higher mortality rates in comparison to male mice. However, whether this is due to an inability to control initial parasite multiplication or due to detrimental effects of the [...] Read more.
Studies indicate that female mice are more susceptible to T. gondii infection, as defined by higher mortality rates in comparison to male mice. However, whether this is due to an inability to control initial parasite multiplication or due to detrimental effects of the immune system has not been determined. Therefore, the following studies were undertaken to determine the influence of sex on early parasite multiplication and the immune response during T. gondii infection and to correlate this with disease outcome. Early parasite replication was studied through applying an in vivo imaging system (IVIS) with luciferase expressing T. gondii. In parallel immunological events were studied by cytometric bead array to quantify key immunological mediators. The results confirmed the previous findings that female mice are more susceptible to acute infection, as determined by higher mortality rates and weight loss compared with males. However, conflicting with expectations, female mice had lower parasite burdens during the acute infection than male mice. Female mice also exhibited significantly increased production of Monocyte Chemoattractant Protein-1 (MCP-1), Interferon (IFN)-γ, and Tumour Necrosis Factor (TNF)-α than male mice. MCP-1 was found to be induced by T. gondii in a dose dependent manner suggesting that the observed increased levels detected in female mice was due to a host-mediated sex difference rather than due to parasite load. However, MCP-1 was not affected by physiological concentration of estrogen or testosterone, indicating that MCP-1 differences observed between the sexes in vivo are due to an as yet unidentified intermediary factor that in turn influences MCP-1 levels. These results suggest that a stronger immune response in female mice compared with male mice enhances their ability to control parasite replication but increases their morbidity and mortality. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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14 pages, 5877 KiB  
Article
Infection with Hymenolepis diminuta Blocks Colitis and Hastens Recovery While Colitis Has Minimal Impact on Expulsion of the Cestode from the Mouse Host
by Shuhua Li, Sruthi Rajeev, Arthur Wang and Derek M. McKay
Pathogens 2021, 10(8), 994; https://doi.org/10.3390/pathogens10080994 - 6 Aug 2021
Cited by 3 | Viewed by 2401
Abstract
Two experimental paradigms were adopted to explore host–helminth interactions involved in the regulation of colitis and to understand if colitis affects the outcome of helminth infection. First, male BALB/c mice infected with H. diminuta were challenged 4 days later with dinitrobenzene sulphonic acid [...] Read more.
Two experimental paradigms were adopted to explore host–helminth interactions involved in the regulation of colitis and to understand if colitis affects the outcome of helminth infection. First, male BALB/c mice infected with H. diminuta were challenged 4 days later with dinitrobenzene sulphonic acid (DNBS) and necropsied 3 days later. Second, mice were infected with H. diminuta 3 days after DNBS treatment and necropsied 11 or 14 days post-DNBS. Mice were assessed for colitic disease severity and infectivity with H. diminuta upon necropsy. Supporting the concept of helminth therapy, mice are protected from DNBS–colitis when infected with H. diminuta only 4 days previously, along with parallel increases in splenic production of Th2 cytokines. In the treatment regimen, H. diminuta infection produced a subtle, statistically significant, enhanced recovery from DNBS. Mice regained body weight quicker, had normalized colon lengths, and showed no overt signs of disease, in comparison to the DNBS-only mice, some of which displayed signs of mild disease at 14 days post-DNBS. Unexpectedly, colitis did not affect the hosts’ anti-worm response. The impact of inflammatory disease on helminth infection is deserving of study in a variety of models as auto-inflammatory diseases emerge in world regions where parasitic helminths are endemic. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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13 pages, 1803 KiB  
Article
Tamoxifen Suppresses the Immune Response to Plasmodium berghei ANKA and Exacerbates Symptomatology
by Luis Antonio Cervantes-Candelas, Jesús Aguilar-Castro, Fidel Orlando Buendía-González, Omar Fernández-Rivera, Armando Cervantes-Sandoval, Jorge Morales-Montor and Martha Legorreta-Herrera
Pathogens 2021, 10(6), 743; https://doi.org/10.3390/pathogens10060743 - 12 Jun 2021
Cited by 4 | Viewed by 3290
Abstract
Malaria is the most lethal parasitic disease in the world. Mortality and severity in symptoms are higher in men than women, suggesting that oestrogens, which are in higher concentration in females than in males, may regulate the immune response against malaria. Tamoxifen, a [...] Read more.
Malaria is the most lethal parasitic disease in the world. Mortality and severity in symptoms are higher in men than women, suggesting that oestrogens, which are in higher concentration in females than in males, may regulate the immune response against malaria. Tamoxifen, a selective oestrogen receptor modulator used in breast cancer treatment due to its antagonistic effect on oestrogen receptors α and β, is also studied because of its potential therapeutic use for several parasitic diseases. However, most studies, including one in malaria, have not addressed the immunomodulatory role of tamoxifen. In this work, we evaluated the effect of tamoxifen on the immune response of CBA/Ca mice against Plasmodium berghei ANKA. This study showed for the first time that tamoxifen increased parasite load, aggravated symptoms by decreasing body temperature and body weight, and worsened anaemia. Additionally, tamoxifen significantly increased the splenic index and the percentages of CD4+ and NK+ cells on day eight post-infection. By contrast, tamoxifen decreased both CD8+ and B220+ populations in the spleen and decreased the serum levels of IL-2, IL-6, and IL-17. Our findings support the notion that tamoxifen is a potent immunomodulator in malaria-infected mice and suggest caution when administering it to malaria-infected women with breast cancer. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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Review

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14 pages, 1808 KiB  
Review
Tick Immunobiology and Extracellular Traps: An Integrative Vision to Control of Vectors
by Hugo Aguilar-Díaz, Rosa Estela Quiroz-Castañeda, Karina Salazar-Morales, Raquel Cossío-Bayúgar and Estefan Miranda-Miranda
Pathogens 2021, 10(11), 1511; https://doi.org/10.3390/pathogens10111511 - 19 Nov 2021
Cited by 7 | Viewed by 3818
Abstract
Ticks are hematophagous ectoparasites that infest a diverse number of vertebrate hosts. The tick immunobiology plays a significant role in establishing and transmitting many pathogens to their hosts. To control tick infestations, the acaricide application is a commonly used method with severe environmental [...] Read more.
Ticks are hematophagous ectoparasites that infest a diverse number of vertebrate hosts. The tick immunobiology plays a significant role in establishing and transmitting many pathogens to their hosts. To control tick infestations, the acaricide application is a commonly used method with severe environmental consequences and the selection of tick-resistant populations. With these drawbacks, new tick control methods need to be developed, and the immune system of ticks contains a plethora of potential candidates for vaccine design. Additionally, tick immunity is based on an orchestrated action of humoral and cellular immune responses. Therefore, the actors of these responses are the object of our study in this review since they are new targets in anti-tick vaccine design. We present their role in the immune response that positions them as feasible targets that can be blocked, inhibited, interfered with, and overexpressed, and then elucidate a new method to control tick infestations through the development of vaccines. We also propose Extracellular Traps Formation (ETosis) in ticks as a process to eliminate their natural enemies and those pathogens they transmit (vectorial capacity), which results attractive since they are a source of acting molecules with potential use as vaccines. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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22 pages, 1119 KiB  
Review
Immunosuppression in Malaria: Do Plasmodium falciparum Parasites Hijack the Host?
by Carlos Lamsfus Calle, Benjamin Mordmüller and Anurag Singh
Pathogens 2021, 10(10), 1277; https://doi.org/10.3390/pathogens10101277 - 3 Oct 2021
Cited by 20 | Viewed by 5042
Abstract
Malaria reflects not only a state of immune activation, but also a state of general immune defect or immunosuppression, of complex etiology that can last longer than the actual episode. Inhabitants of malaria-endemic regions with lifelong exposure to the parasite show an exhausted [...] Read more.
Malaria reflects not only a state of immune activation, but also a state of general immune defect or immunosuppression, of complex etiology that can last longer than the actual episode. Inhabitants of malaria-endemic regions with lifelong exposure to the parasite show an exhausted or immune regulatory profile compared to non- or minimally exposed subjects. Several studies and experiments to identify and characterize the cause of this malaria-related immunosuppression have shown that malaria suppresses humoral and cellular responses to both homologous (Plasmodium) and heterologous antigens (e.g., vaccines). However, neither the underlying mechanisms nor the relative involvement of different types of immune cells in immunosuppression during malaria is well understood. Moreover, the implication of the parasite during the different stages of the modulation of immunity has not been addressed in detail. There is growing evidence of a role of immune regulators and cellular components in malaria that may lead to immunosuppression that needs further research. In this review, we summarize the current evidence on how malaria parasites may directly and indirectly induce immunosuppression and investigate the potential role of specific cell types, effector molecules and other immunoregulatory factors. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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20 pages, 3250 KiB  
Review
Enteric Tuft Cells in Host-Parasite Interactions
by Sruthi Rajeev, Olivia Sosnowski, Shuhua Li, Thibault Allain, André G. Buret and Derek M. McKay
Pathogens 2021, 10(9), 1163; https://doi.org/10.3390/pathogens10091163 - 9 Sep 2021
Cited by 11 | Viewed by 4446
Abstract
Enteric tuft cells are chemosensory epithelial cells gaining attention in the field of host-parasite interactions. Expressing a repertoire of chemosensing receptors and mediators, these cells have the potential to detect lumen-dwelling helminth and protozoan parasites and coordinate epithelial, immune, and neuronal cell defenses [...] Read more.
Enteric tuft cells are chemosensory epithelial cells gaining attention in the field of host-parasite interactions. Expressing a repertoire of chemosensing receptors and mediators, these cells have the potential to detect lumen-dwelling helminth and protozoan parasites and coordinate epithelial, immune, and neuronal cell defenses against them. This review highlights the versatility of enteric tuft cells and sub-types thereof, showcasing nuances of tuft cell responses to different parasites, with a focus on helminths reflecting the current state of the field. The role of enteric tuft cells in irritable bowel syndrome, inflammatory bowel disease and intestinal viral infection is assessed in the context of concomitant infection with parasites. Finally, the review presents pertinent questions germane to understanding the enteric tuft cell and its role in enteric parasitic infections. There is much to be done to fully elucidate the response of this intriguing cell type to parasitic-infection and there is negligible data on the biology of the human enteric tuft cell—a glaring gap in knowledge that must be filled. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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21 pages, 862 KiB  
Review
Trichuris muris Model: Role in Understanding Intestinal Immune Response, Inflammation and Host Defense
by Yeganeh Yousefi, Sabah Haq, Suhrid Banskota, Yun Han Kwon and Waliul I. Khan
Pathogens 2021, 10(8), 925; https://doi.org/10.3390/pathogens10080925 - 22 Jul 2021
Cited by 12 | Viewed by 5901
Abstract
Several parasites have evolved to survive in the human intestinal tract and over 1 billion people around the world, specifically in developing countries, are infected with enteric helminths. Trichuris trichiura is one of the world’s most common intestinal parasites that causes human parasitic [...] Read more.
Several parasites have evolved to survive in the human intestinal tract and over 1 billion people around the world, specifically in developing countries, are infected with enteric helminths. Trichuris trichiura is one of the world’s most common intestinal parasites that causes human parasitic infections. Trichuris muris, as an immunologically well-defined mouse model of T. trichiura, is extensively used to study different aspects of the innate and adaptive components of the immune system. Studies on T. muris model offer insights into understanding host immunity, since this parasite generates two distinct immune responses in resistant and susceptible strains of mouse. Apart from the immune cells, T. muris infection also influences various components of the intestinal tract, especially the gut microbiota, mucus layer, epithelial cells and smooth muscle cells. Here, we reviewed the different immune responses generated by innate and adaptive immune components during acute and chronic T. muris infections. Furthermore, we discussed the importance of studying T. muris model in understanding host–parasite interaction in the context of alteration in the host’s microbiota, intestinal barrier, inflammation, and host defense, and in parasite infection-mediated modulation of other immune and inflammatory diseases. Full article
(This article belongs to the Special Issue Advances in the Immunobiology of Parasitic Diseases)
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