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Review
.2015 Jun 30:6:666.
doi: 10.3389/fmicb.2015.00666. eCollection 2015.

Infection-related hemolysis and susceptibility to Gram-negative bacterial co-infection

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Review

Infection-related hemolysis and susceptibility to Gram-negative bacterial co-infection

Katharine Orf et al. Front Microbiol..

Abstract

Increased susceptibility to co-infection with enteric Gram-negative bacteria, particularly non-typhoidal Salmonella, is reported in malaria and Oroya fever (Bartonella bacilliformis infection), and can lead to increased mortality. Accumulating epidemiological evidence indicates a causal association with risk of bacterial co-infection, rather than just co-incidence of common risk factors. Both malaria and Oroya fever are characterized by hemolysis, and observations in humans and animal models suggest that hemolysis causes the susceptibility to bacterial co-infection. Evidence from animal models implicates hemolysis in the impairment of a variety of host defense mechanisms, including macrophage dysfunction, neutrophil dysfunction, and impairment of adaptive immune responses. One mechanism supported by evidence from animal models and human data, is the induction of heme oxygenase-1 in bone marrow, which impairs the ability of developing neutrophils to mount a competent oxidative burst. As a result, dysfunctional neutrophils become a new niche for replication of intracellular bacteria. Here we critically appraise and summarize the key evidence for mechanisms which may contribute to these very specific combinations of co-infections, and propose interventions to ameliorate this risk.

Keywords: Babesiosis; Bartonellosis; Salmonella; co-infection; heme oxygenase; hemolysis; malaria.

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Figures

Figure 1
Figure 1
Mechanisms and consequences of hemolysis. The fate of the contents of red blood cells (RBCs) depends on whether hemolysis is extravascular or intravascular. Following intravascular hemolysis, hemoglobion (Hb) is bound by haptoglobin and taken up by monocytes and macrophages. When haptoglobin is depleted, heme is released from Hb and is bound by hemopexin. The heme-hemopexin complex is primarily cleared by macrophages and hepatocytes. If hemolysis overwhelms the capacity of both haptoglobin and hemopexin, heme remains within the circulation, weakly binding to albumin and lipoproteins, and can interact with other cell types. In extravascular hemolysis, red blood cells are removed by phagocytic cells, primarily in the spleen and liver. Heme released from both intra- and extravascular hemolysis induces the expression of heme oxygenase-1 (HO-1), which degrades heme to iron, biliverdin, and carbon monoxide.
Figure 2
Figure 2
Mechanisms controlling invasion and dissemination of non-typhoidalSalmonella(NTS). NTS invades across the intestinal mucosa, into the submucosal tissues where a local inflammatory cell infiltrate may limit further invasion. If they evade this response, the bacteria disseminate through the blood and lymphatics, and reach phagocytic cells in the spleen and liver, where they may evade killing and replicate. Both hemolysis in general, and malaria, impair host defense mechanisms at each stage of NTS infection. Mechanisms which are likely to be general consequences of intravascular hemolysis are underlined and those that are likely malaria-specific are not underlined.
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