No infection is bad. Infection response is good or bad. Your survival depends upon how you respond. Killing microbes, killing worms is no way right response. As shared in this research, worms are actually having serious talk with our immune system. Our killing hampers communication and so there will be another spell of infection and the vicious cycle goes on,. Ideal response is to make this talk efficient and while the talk is going on, maintain bodily प्राण. And the response is based on our innate energy layer i.e. प्राणमय कोष (प्राणिक शरीर). Richer the प्राण, better the response.
Otherwise, no infection is bad. All infections have goal/purpose, designed by nature, to help the host organisms to emerge as more strongly typed identities (Self-realization, Ego, “I”-ness – whatever way you understand)
Since children are growing and their I-ness is developing, they frequently get infections.
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Researchers have discovered how intestinal worm infections cross-talk with gut bacteria to help the immune system. Intestinal worms infect over 2 billion people across the world, mostly children, in areas with poor sanitation. But despite causing serious health problems, worms can actually help the immune system of its host as an indirect way of protecting themselves, say authors of the new report.
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For last 100 years, we are groomed to treat non-self as enemy, mother nature as enemy and we are always engaged in unnecessarily war-like responses i.e antibiotics and vaccines.
Research
The Intestinal Microbiota Contributes to the Ability of Helminths to Modulate Allergic Inflammation.
http://www.cell.com/immunity/abstract/S1074-7613(15)00397-0
Highlights
- •The microbiota contributes to helminth-induced modulation of allergic asthma
- •Cecal microbial communities are altered in helminth-infected mice
- •Helminth infection increases microbial-derived short chain fatty acids
- •GPR41 mediates helminth-induced Treg cell suppressor function
Summary
Intestinal helminths are potent regulators of their host’s immune system and can ameliorate inflammatory diseases such as allergic asthma. In the present study we have assessed whether this anti-inflammatory activity was purely intrinsic to helminths, or whether it also involved crosstalk with the local microbiota. We report that chronic infection with the murine helminth Heligmosomoides polygyrus bakeri (Hpb) altered the intestinal habitat, allowing increased short chain fatty acid (SCFA) production. Transfer of the Hpb-modified microbiota alone was sufficient to mediate protection against allergic asthma. The helminth-induced anti-inflammatory cytokine secretion and regulatory T cell suppressor activity that mediated the protection required the G protein-coupled receptor (GPR)-41. A similar alteration in the metabolic potential of intestinal bacterial communities was observed with diverse parasitic and host species, suggesting that this represents an evolutionary conserved mechanism of host-microbe-helminth interactions.
