Efficient control of Leishmania and Strongyloides despite partial suppression of nematode‐induced Th2 response in co‐infected mice

Abstract

Endemic regions for the pathogenic nematode Strongyloides and parasitic protist Leishmania overlap and therefore co-infections with both parasites frequently occur. As the Th2 and Th1 immune responses necessary to efficiently control Strongyloides and Leishmania infections are known to counterregulate each other, we analysed the outcome of co-infection in the murine system. Here, we show that Leishmania major-specific Th1 responses partially suppressed the nematode-induced Th2 response in co-infected mice. Despite this modulation, successful expulsion of gut dwelling Strongyloides was not suppressed in mice with pre-existing or subsequent Leishmania infection. A pre-existing Strongyloides infection, in contrast, did not interfere with efficient type-1 responses but even increased pro-inflammatory cytokine production. Also, control of L. major infections was not affected by pre-existing nematode infection. Taken together, we provide evidence that simultaneous presence of helminth and protist parasites did not interfere with efficient host defence in our co-infection model.

Intestinal nematode infection exacerbates experimental visceral leishmaniasis

“…This dichotomy is not as clear in the case of L donovani infections, and like many other infectious organisms, L donovani has immune‐modulating capacities . Despite what we know of the balance and antagonism between T‐cell subsets, outcomes of coinfection models and clinical studies addressing this subject have not always been predictable . In an experimental VL model where BALB/c mice were infected with Leishmania infantum seven days after Trichinella spiralis infection, coinfected mice had higher Leishmania burden, but surprisingly, IFN‐γ production was also elevated .…”

“…19 Despite what we know of the balance and antagonism between T-cell subsets, outcomes of coinfection models and clinical studies addressing this subject have not always been predictable. 20,21 In an experimental VL model where BALB/c mice were infected with Leishmania infantum seven days after Trichinella spiralis infection, coinfected mice had higher Leishmania burden, but surprisingly, IFNγ production was also elevated. 20 In contrast, preexisting, acute Strongyloides ratti infection was found not to affect L major lesions in C57BL/6 mice despite hampered IFNγ levels in draining lymph nodes.…”

“…20 In contrast, preexisting, acute Strongyloides ratti infection was found not to affect L major lesions in C57BL/6 mice despite hampered IFNγ levels in draining lymph nodes. 21 burdens are high [24][25][26][27] and when the worm itself is in proximity to the secondary challenge. 24 Lymphocytes are rare in healthy hepatic tissue of young SPF mice, 28 and as expected, the H. polygyrus infection alone did not affect expression of T cell-associated mRNAs in the liver.…”

IgG Antibody responses in mice coinfected with Toxocara canis and other helminths or protozoan parasites

“…From the experimental point of view and also under a theoretical perspective, there are several studies on the interactions among parasites harbored by the same host reporting either competitive action, development of cross-immunity, synergy or indifferent coexistence 7,28 . In certain circumstances, changes that take place among organisms of different species that live as parasites on the same host manifest negative interactions increasing the immune response against a second parasite by means of cross-immunity or, conversely, cause immunosuppression of the host, thus showing a positive interaction 10 .…”

Chronic Gastrointestinal Nematode Infection Mutes Immune Responses to Mycobacterial Infection Distal to the Gut

“…However, the impact helminths have on vaccine efficacy and other secondary infections remains an open question. Indeed, a number of studies report a lack of correlation between intestinal worms and secondary infections (10)(11)(12)(13). In common for many of the studies describing an association between worms and increased susceptibility to secondary infection, or reduced inflammatory response in experimental autoimmune disease, is that the effects have been observed in tissue (s) in direct or close contact with the worm (14,15).…”