PubMed · 4123160
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M H Hambling. 1973-06-30. The devil's grip.. https://doi.org/10.1016/s0140-6736(73)91836-9
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Infections by coxsackie virus B3 (CVB3) have been reported to be associated with an enhanced influx of mononuclear leukocytes into afflicted tissue. Current evidence indicates that monocytes/macrophages are specifically involved in CVB3-induced myocarditis by maintaining a chronic inflammatory response. To examine susceptibility and reactivity to CVB3, freshly isolated human monocytes were exposed to various virus doses (0.1-10 MOI) in the presence or absence of macrophage-activating lipopolysaccharide (LPS). CVB3 infection alone induced an activation of monocytes as evidenced by enhanced adherence, release of cytokines and secretion of prostaglandin E2 (PGE2). Simultaneous addition of LPS almost entirely suppressed LPS-specific production of tumour necrosis factor alpha (TNF alpha) and PGE2, partially inhibited release of interleukin 1 beta (IL 1 beta) and did not affect interleukin 6 (IL6) synthesis of CVB3-infected monocytes. These data show that CVB3 activates monocytes to cytokine production but renders them unreactive to further activating stimuli. Further studies should determine the extent to which continuous cytokine release from persistently CVB3-infected monocytes, and their apparent unresponsiveness to other stimuli, contribute to chronic myocarditis.
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Coxsackievirus B3 (CVB3) infections produce an inflammatory and immune response that suggests the involvement of cytokines. In this in vitro study, we exposed purified human monocytes to CVB3 and determined the release of interferon (IFN), interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha). Exposure to CVB3 did not alter the viability of monocytes, however, it induced an increased adherence. After 12 and 24 h of CVB3 exposure, monocytes released large amounts of IFN, IL-1 beta and TNF-alpha. These data show that CVB3 strongly affects human monocytes and activates them to production of biologically active cytokines, particularly IL-1 beta and TNF-alpha. It is suggested that both cytokines, when released in large amounts and for a prolonged period, may contribute to a strong inflammatory response and eventual tissue damage in afflicted organs such as the myocardium.