Acute helminth infection enhances early macrophage mediated control of mycobacterial infection

Plessis, Nelita du; Kleynhans, Léanie; Thiart, Leani; Helden, Paul D. van; Brombacher, Frank; Horsnell, William G. C.; Walzl, Gerhard

doi:10.1038/mi.2012.131

Cited by 38 publications

(38 citation statements)

References 59 publications

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“…The mechanistic basis for the enhanced-susceptibility to M. tuberculosis of those coinfected mice was mainly IL-4 receptor–mediated alternative activation of macrophages. In contrast, another study has reported that acute infection with N. brasiliensis actually boosts early macrophage-mediated control of infection with BCG 34 . However, it must be noted that BCG does not express certain genes 35 encoding molecules that control the virulence and intracellular survival of mycobacteria 36 ; therefore, it is not clear that such a boosting effect would occur during infection with M. tuberculosis .…”

Section: Tuberculosis and Concurrent Helminth Infectionmentioning

confidence: 85%

Effect of helminth-induced immunity on infections with microbial pathogens

2013

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Helminth infections are ubiquitous worldwide and can trigger potent immune responses that differ from and potentially antagonize host protective responses to microbial pathogens. In this Review we focus on the three main killers in infectious disease—AIDS, tuberculosis and malaria—and critically assesses whether helminths adversely influence host control of these diseases. We also discuss emerging concepts for how M2 macrophages and helminth-modulated dendritic cells can potentially influence the protective immune response to concurrent infections. Finally, we present evidence advocating for more efforts to determine how and to what extent helminths interfere with the successful control of specific concurrent coinfections.

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Section: Tuberculosis and Concurrent Helminth Infectionmentioning

confidence: 85%

Effect of helminth-induced immunity on infections with microbial pathogens

2013

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“…Previous studies suggest that early innate recognition of bacteria has the potential to overcome the normally detrimental impact of helminth infection on resistance to bacterial infection [44,45]. Furthermore helminth expanded resident MΦ have been shown to exert a protective effect in models of sepsis [46,47].…”

Section: Discussionmentioning

confidence: 99%

Macrophage origin limits functional plasticity in helminth-bacterial co-infection

et al. 2017

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Rapid reprogramming of the macrophage activation phenotype is considered important in the defense against consecutive infection with diverse infectious agents. However, in the setting of persistent, chronic infection the functional importance of macrophage-intrinsic adaptation to changing environments vs. recruitment of new macrophages remains unclear. Here we show that resident peritoneal macrophages expanded by infection with the nematode Heligmosomoides polygyrus bakeri altered their activation phenotype in response to infection with Salmonella enterica ser. Typhimurium in vitro and in vivo. The nematode-expanded resident F4/80high macrophages efficiently upregulated bacterial induced effector molecules (e.g. MHC-II, NOS2) similarly to newly recruited monocyte-derived macrophages. Nonetheless, recruitment of blood monocyte-derived macrophages to Salmonella infection occurred with equal magnitude in co-infected animals and caused displacement of the nematode-expanded, tissue resident-derived macrophages from the peritoneal cavity. Global gene expression analysis revealed that although nematode-expanded resident F4/80high macrophages made an anti-bacterial response, this was muted as compared to newly recruited F4/80low macrophages. However, the F4/80high macrophages adopted unique functional characteristics that included enhanced neutrophil-stimulating chemokine production. Thus, our data provide important evidence that plastic adaptation of MΦ activation does occur in vivo, but that cellular plasticity is outweighed by functional capabilities specific to the tissue origin of the cell.

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“…Interestingly, IL-4 and IL-10 deficiency was necessary to reverse the obstructing effect of H. polygyrus infection on the CD8 + T cell response toward Toxoplasma (Marple et al, 2017). The majority of co-infection studies despite being protozoan, viral or bacterial infection, have focused on infections with helminth first due to their ability to downmodulate immune responses (Rousseau et al, 1997; Liesenfeld et al, 2004; Chen et al, 2005, 2006; Graham et al, 2005; Su et al, 2005, 2014a,b; Weng et al, 2007; Khan et al, 2008; Noland et al, 2008; Miller et al, 2009; Frantz et al, 2010; Dias et al, 2011; Potian et al, 2011; Kolbaum et al, 2012; du Plessis et al, 2013; Osborne et al, 2014; Budischak et al, 2015; Coomes et al, 2015; Gondorf et al, 2015; Rafi et al, 2015; Obieglo et al, 2016). In light of the fact, that Th2 immunity against helminths is an ongoing challenge in humans and livestock, we aimed to investigate how a previous protozoan infection affects the development of Th2 responses in CD4 + T cells and protection against helminths.…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma Co-infection Prevents Th2 Differentiation and Leads to a Helminth-Specific Th1 Response

Ahmed

French

Kühl³

et al. 2017

Front. Cell. Infect. Microbiol.

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Nematode infections, in particular gastrointestinal nematodes, are widespread and co-infections with other parasites and pathogens are frequently encountered in humans and animals. To decipher the immunological effects of a widespread protozoan infection on the anti-helminth immune response we studied a co-infection with the enteric nematode Heligmosomoides polygyrus in mice previously infected with Toxoplasma gondii. Protective immune responses against nematodes are dependent on parasite-specific Th2 responses associated with IL-4, IL-5, IL-13, IgE, and IgG1 antibodies. In contrast, Toxoplasma gondii infection elicits a strong and protective Th1 immune response characterized by IFN-γ, IL-12, and IgG2a antibodies. Co-infected animals displayed significantly higher worm fecundity although worm burden remained unchanged. In line with this, the Th2 response to H. polygyrus in co-infected animals showed a profound reduction of IL-4, IL-5, IL-13, and GATA-3 expressing T cells. Co-infection also resulted in the lack of eosinophilia and reduced expression of the Th2 effector molecule RELM-β in intestinal tissue. In contrast, the Th1 response to the protozoan parasite was not diminished and parasitemia of T. gondii was unaffected by concurrent helminth infection. Importantly, H. polygyrus specific restimulation of splenocytes revealed H. polygyrus-reactive CD4+ T cells that produce a significant amount of IFN-γ in co-infected animals. This was not observed in animals infected with the nematode alone. Increased levels of H. polygyrus-specific IgG2a antibodies in co-infected mice mirrored this finding. This study suggests that polarization rather than priming of naive CD4+ T cells is disturbed in mice previously infected with T. gondii. In conclusion, a previous T. gondii infection limits a helminth-specific Th2 immune response while promoting a shift toward a Th1-type immune response.

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Acute helminth infection enhances early macrophage mediated control of mycobacterial infection

Cited by 38 publications

References 59 publications

Effect of helminth-induced immunity on infections with microbial pathogens

Effect of helminth-induced immunity on infections with microbial pathogens

Macrophage origin limits functional plasticity in helminth-bacterial co-infection

Toxoplasma Co-infection Prevents Th2 Differentiation and Leads to a Helminth-Specific Th1 Response

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