Manuel Kulagin

born in dresden, germany

lived in heidelberg for 13years

living in chernex, switzerland since 2002

2 children (1st born in 2006, 2nd in 2009)

obtained cfc/maturité at the ESS Lausanne in 2009 as laboratory technician

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Helminthiase

Une helminthiase est un terme désignant les maladies parasitaires, causées par des vers parasites intestinaux, les helminthes. Ces vers constituent un important problème de santé publique dans les pa

Hookworms Evade Host Immunity by Secreting a Deoxyribonuclease to Degrade Neutrophil Extracellular Traps

Tiffany Babette Angélique Bouchery, Romain Guiet, Nicola Harris, Manuel Kulagin, Mati André Marie Moyat, Arne Seitz, Kathleen Shah, Beatrice Volpe

Hookworms cause a major neglected tropical disease, occurring after larvae penetrate the host skin. Neutrophils are phagocytes that kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they target hookworms during skin infection is unknown. Using a murine hookworm, Nippostrongylus brasiliensis, we observed neutrophils being rapidly recruited and deploying NETs around skin-penetrating larvae. Neutrophils depletion or NET inhibition altered larvae behavior and enhanced the number of adult worms following murine infection. Nevertheless, larvae were able to mitigate the effect of NETs by secreting a deoxyribonuclease (NbDNase II) to degrade the DNA backbone. Critically, neutrophils were able to kill larvae in vitro, which was enhanced by neutralizing Nb-DNase II. Homologs of Nb-DNase II are present in other nematodes, including the human hookworm, Necator americanus, which also evaded NETs in vitro. These findings highlight the importance of neutrophils in hookworm infection and a potential conserved mechanism of immune evasion.

CELL PRESS2020

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Inflammatory arthritis and systemic bone loss are attenuated by gastrointestinal helminth parasites

Nicola Harris, Manuel Kulagin, Mario Michael Zaiss

Infections with different helminth species have been observed to ameliorate a variety of chronic inflammatory diseases. Herein, we show that the natural murine helminth species, Heligmosomoides polygyrus bakeri (Hp) is capable of attenuating disease severity in two different inflammatory arthritis models. Furthermore, we show that excretory-secretory (ES) products from Hp directly suppress osteoclast differentiation in vitro. Taken together, these results demonstrate that helminth infections can dampen autoimmune diseases and highlight a previously unrecognized and important role for ES products, by directly impacting on bone destruction.

Taylor & Francis2017

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Antibody-Mediated Trapping of Helminth Larvae Requires CD11b and Fc gamma Receptor I

Julia Esser-von Bieren, Romain Guiet, Nicola Harris, Manuel Kulagin, Benjamin John Marsland, Arne Seitz, Duncan-Bruce Sutherland, Beatrice Volpe

Infections with intestinal helminths severely impact on human and veterinary health, particularly through the damage that these large parasites inflict when migrating through host tissues. Host immunity often targets the motility of tissue-migrating helminth larvae, which ideally should be mimicked by anti-helminth vaccines. However, the mechanisms of larval trapping are still poorly defined. We have recently reported an important role for Abs in the rapid trapping of tissue-migrating larvae of the murine parasite Heligmosomoides polygyrus bakeri. Trapping was mediated by macrophages (M Phi) and involved complement, activating FcRs, and Arginase-1 (Arg1) activity. However, the receptors and Ab isotypes responsible for M Phi adherence and Arg1 induction remained unclear. Using an in vitro coculture assay of H. polygyrus bakeri larvae and bone marrow-derived M Phi, we now identify CD11b as the major complement receptor mediating M Phi adherence to the larval surface. However, larval immobilization was largely independent of CD11b and instead required the activating IgG receptor Fc gamma RI (CD64) both in vitro and during challenge H. polygyrus bakeri infection in vivo. Fc gamma RI signaling also contributed to the upregulation of M Phi Arg1 expression in vitro and in vivo. Finally, IgG2a/c was the major IgG subtype from early immune serum bound by FcgRI on the M Phi surface, and purified IgG2c could trigger larval immobilization and Arg1 expression in M Phi in vitro. Our findings reveal a novel role for IgG2a/c-Fc gamma RI-driven M Phi activation in the efficient trapping of tissue-migrating helminth larvae and thus provide important mechanistic insights vital for anti-helminth vaccine development.

Amer Assoc Immunologists2015

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