Excretory-secretory products from adult helminth have bactericidal activity.

Intestinal helminths and microbiota share the same anatomical niche during infection and are likely to interact either directly or indirectly. Whether intestinal helminths employ bactericidal strategies that influence their microbial environment is not completely understood. In the present study, the hypothesis that the adult hookworm produces molecules that impair bacterial growth , is tested.

Induction of Siglec-FCD101 eosinophils in the lungs following murine hookworm infection.

Helminth-induced eosinophils accumulate around the parasite at the site of infection, or in parasite-damaged tissues well after the helminth has left the site. The role of helminth-elicited eosinophils in mediating parasite control is complex. While they may contribute to direct parasite-killing and tissue repair, their involvement in long-term immunopathogenesis is a concern.

Hookworm infection associates with a vaginal Type 1/Type 2 immune signature and increased HPV load.

Helminth infection-driven changes to immunity in the female reproductive tract (FRT) is an immune axis that is currently understudied but can have major implications for the control of FRT infections. Here we address how human hookworm infection associates with vaginal immune profile and risk of Human papillomavirus (HPV) infection. Stool, blood, cervical swabs and vaginal flushes were collected from women from the Central region of Togo to screen for hookworms ( and high carcinogenic risk HPV types, Kato Katz and PCR, respectively.

Differential Regulation of Allergic Airway Inflammation by Acetylcholine.

Acetylcholine (ACh) from neuronal and non-neuronal sources plays an important role in the regulation of immune responses and is associated with the development of several disease pathologies. We have previously demonstrated that group 2 innate lymphoid cell (ILC2)-derived ACh is required for optimal type 2 responses to parasitic infection and therefore sought to determine whether this also plays a role in allergic inflammation. mice (in which ILC2s cannot synthesize ACh) were exposed to an allergenic extract of the fungus , and immune responses in the airways and lung tissues were analyzed.

Helminths are positively AMPing up gut de-bugging.

In recently published work, Hu, Zhang, and colleagues identify SPRR2A as a novel intestinal antimicrobial protein (AMP) that targets Gram-positive bacteria (Hu et al., 2021). Unexpectedly, the authors show that SPRR2A is induced by helminth-elicited type 2 immunity to restrict pathogenic bacteria translocation across the helminth-infection-damaged epithelium.

Ascaris exposure and its association with lung function, asthma, and DNA methylation in Northern Europe.

Background: Ascaris infections, with a worldwide prevalence above 10%, can cause respiratory pathology. However, long-term effects on lung function in humans are largely unknown.

Objective: We investigated the associations of Ascaris exposure with lung function, asthma, and DNA methylation.

Inherent maternal type 2 immunity: Consequences for maternal and offspring health.

An inherent elevation in type 2 immunity is a feature of maternal and offspring immune systems. This has diverse implications for maternal and offspring biology including influencing success of pregnancy, offspring immune development and maternal and offspring ability to control infection and diseases such as allergies. In this review we provide a broad insight into how this immunological feature of pregnancy and early life impacts both maternal and offspring biology.

Il4ra-independent vaginal eosinophil accumulation following helminth infection exacerbates epithelial ulcerative pathology of HSV-2 infection.

How helminths influence the pathogenesis of sexually transmitted viral infections is not comprehensively understood. Here, we show that an acute helminth infection (Nippostrongylus brasiliensis [Nb]) induced a type 2 immune profile in the female genital tract (FGT). This leads to heightened epithelial ulceration and pathology in subsequent herpes simplex virus (HSV)-2 infection.

Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths.

Innate lymphoid cells (ILCs) are critical mediators of immunological and physiological responses at mucosal barrier sites. Whereas neurotransmitters can stimulate ILCs, the synthesis of small-molecule neurotransmitters by these cells has only recently been appreciated. Group 2 ILCs (ILC2s) are shown here to synthesize and release acetylcholine (ACh) during parasitic nematode infection.

Immune serum-activated human macrophages coordinate with eosinophils to immobilize Ascaris suum larvae.

Helminth infection represents a major health problem causing approximately 5 million disability-adjusted life years worldwide. Concerns that repeated anti-helminthic treatment may lead to drug resistance render it important that vaccines are developed but will require increased understanding of the immune-mediated cellular and antibody responses to helminth infection. IL-4 or antibody-activated murine macrophages are known to immobilize parasitic nematode larvae, but few studies have addressed whether this is translatable to human macrophages.

Pre-conception maternal helminth infection transfers via nursing long-lasting cellular immunity against helminths to offspring.

Maternal immune transfer is the most significant source of protection from early-life infection, but whether maternal transfer of immunity by nursing permanently alters offspring immunity is poorly understood. Here, we identify maternal immune imprinting of offspring nursed by mothers who had a pre-conception helminth infection. Nursing of pups by helminth-exposed mothers transferred protective cellular immunity to these offspring against helminth infection.

Sterile Lung Inflammation Induced by Silica Exacerbates Mycobacterium tuberculosis Infection via STING-Dependent Type 2 Immunity.

Lung inflammation induced by silica impairs host control of tuberculosis, yet the underlying mechanism remains unclear. Here, we show that silica-driven exacerbation of M. tuberculosis infection associates with raised type 2 immunity.

Helminth-induced IL-4 expands bystander memory CD8 T cells for early control of viral infection.

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8 T cells (T) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the T compartment.

Hookworm exposure decreases human papillomavirus uptake and cervical cancer cell migration through systemic regulation of epithelial-mesenchymal transition marker expression.

Persistent infection with human papillomavirus (HPV) is responsible for nearly all new cervical cancer cases worldwide. In low- and middle-income countries (LMIC), infection with helminths has been linked to increased HPV prevalence. As the incidence of cervical cancer rises in helminth endemic regions, it is critical to understand the interaction between exposure to helminths and the progression of cervical cancer.

Chronic schistosomiasis suppresses HIV-specific responses to DNA-MVA and MVA-gp140 Env vaccine regimens despite antihelminthic treatment and increases helminth-associated pathology in a mouse model.

Future HIV vaccines are expected to induce effective Th1 cell-mediated and Env-specific antibody responses that are necessary to offer protective immunity to HIV infection. However, HIV infections are highly prevalent in helminth endemic areas. Helminth infections induce polarised Th2 responses that may impair HIV vaccine-generated Th1 responses.

Elevated IgG Responses in Infants Are Associated With Reduced Prevalence of Infection.

Background: It is unclear whether antibodies can prevent () infection. In this study, we examined the relationship between total plasma IgG levels, IgG elicited by childhood vaccines and soil-transmitted helminths, and infection prevalence, defined by positive QuantiFERON (QFT) test.

Methods: We studied 100 uninfected infants, aged 4-6 months.

Non-Pulmonary Immune Functions of Surfactant Proteins A and D.

Surfactant proteins A (SP-A) and D (SP-D) are established as essential components of our innate immune system for protecting the lung from pathogens and allergens. They essentially exert their protective functions by regulating pulmonary homeostasis. Both proteins are however widely expressed throughout the body, including the female reproductive tract, urinary tract, gastrointestinal tract, the eye, ear, nasal compartment, central nervous system, the coronary artery and the skin.

RELMs in the Realm of Helminths.

Resistin-like molecule (RELM) proteins are essential for immunity to helminths. Recently, Chen and collaborators identified a dominant role for RELMα over RELMβ in host immunity to Nippostrongylus brasiliensis using a double knockout system. The study highlighted how important and yet divergent the contributions of these proteins are in the control of helminth infections.

Surfactant Protein-D Is Essential for Immunity to Helminth Infection.

Pulmonary epithelial cell responses can enhance type 2 immunity and contribute to control of nematode infections. An important epithelial product is the collectin Surfactant Protein D (SP-D). We found that SP-D concentrations increased in the lung following Nippostrongylus brasiliensis infection; this increase was dependent on key components of the type 2 immune response.

Role of IL-4 receptor α-positive CD4(+) T cells in chronic airway hyperresponsiveness.

Background: TH2 cells and their cytokines are associated with allergic asthma in human subjects and with mouse models of allergic airway disease. IL-4 signaling through the IL-4 receptor α (IL-4Rα) chain on CD4(+) T cells leads to TH2 cell differentiation in vitro, implying that IL-4Rα-responsive CD4(+) T cells are critical for the induction of allergic asthma. However, mechanisms regulating acute and chronic allergen-specific TH2 responses in vivo remain incompletely understood.

The M3 muscarinic receptor is required for optimal adaptive immunity to helminth and bacterial infection.

Innate immunity is regulated by cholinergic signalling through nicotinic acetylcholine receptors. We show here that signalling through the M3 muscarinic acetylcholine receptor (M3R) plays an important role in adaptive immunity to both Nippostrongylus brasiliensis and Salmonella enterica serovar Typhimurium, as M3R-/- mice were impaired in their ability to resolve infection with either pathogen. CD4 T cell activation and cytokine production were reduced in M3R-/- mice.

IL-4Rα-associated antigen processing by B cells promotes immunity in Nippostrongylus brasiliensis infection.

In this study, B cell function in protective T(H)2 immunity against N. brasiliensis infection was investigated. Protection against secondary infection depended on IL-4Rα and IL-13; but not IL-4.