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Chapter 11 : The Influence of Helminths on Immunological Diseases
Category: Food Microbiology; Applied and Industrial Microbiology
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Helminths are powerful modulators of host mucosal and systemic immunity. Helminths induce mucosal T cells to make Th2 and regulatory cytokines that participate in the protective process. Helminths affect pathways of innate immunity and induce various regulatory Tcell subsets that limit immune reactivity. The chapter explores the implications of expanding industrialization on the demographics of immunological diseases worldwide. The ‘‘hygiene hypothesis’’ states that immunological diseases may be an unanticipated consequence of improvements in public health and hygiene. Deworming of children and adults, associated with improved public hygiene, could be one of the factors leading to the rise in immunological diseases. People carrying helminths can show immune bias away from the Th1 response normally elicited with tetanus vaccination or in vitro mitogen stimulation. Animal experimentation shows that helminths can prevent the onset of various immunological diseases and reverse ongoing pathology. A case control study in Ethiopia showed a lower frequency of asthma in people infected with hookworm than in uninfected people. Colonization with intestinal helminths protects mice from trinitrobenzene sulfonic acid (TNBS)-induced colitis, which is a Th1-driven disease. It appears that helminths trigger various immunoregulatory pathways to control aberrant inflammation. Helminth colonization can have negative consequences. Some worms can cause disease. Recent experiments using murine and larger animal models suggest that worm infection can interfere with vaccine efficacy. An underlying helminth infection may interfere with the accurate diagnosis of infectious status or leave some animals more susceptible to some serious pathogen-induced enteric infections.
Key Concept Ranking
- Transforming Growth Factor beta
Helminths induce the host’s immune system to produce various regulatory T-cell subtypes. These work through several mechanisms to limit the production and function of Th1, Th2, and Th17 effector T cells that drive immunopathology. Helminths also induce changes in innate immunity that can limit inflammation independently of the adoptive immunity (not shown). TLR4, Toll-like receptor 4.