Necrotising fasciitis in a patient receiving infliximab for rheumatoid arthritis

Chan, Aw; Cleeve, V.; Daymond, T. J.

doi:10.1136/pmj.78.915.47

Cited by 79 publications

(36 citation statements)

References 8 publications

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“…These data suggested that TNF-a, but not IL-1R or TLR2, is involved in host defense against GAS soft tissue infection. Interestingly, these findings are in accordance with reports that anti-TNF-a therapy may increase the risk for GAS NF in rheumatoid arthritis and dermatomyositis patients (31,32).…”

Section: Resultssupporting

confidence: 82%

Recruited Macrophages Control Dissemination of Group A Streptococcus from Infected Soft Tissues

Mishalian

Ordan

Peled³

et al. 2011

The Journal of Immunology

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Group A Streptococcus (GAS) causes diverse infections in humans, ranging from mild to life-threatening invasive diseases, such as necrotizing fasciitis (NF), a rapidly progressing deep tissue infection. Despite prompt treatments, NF remains a significant cause of morbidity and mortality, even in previously healthy individuals. The early recruitment of leukocytes is crucial to the outcome of NF; however, although the role of polymorphonuclear neutrophils (PMNs) in host defense against NF is well established, the role of recruited macrophages remains poorly defined. Using a cutaneous murine model mimicking human NF, we found that mice deficient in TNF-α were highly susceptible to s.c. infections with GAS, and a paucity of macrophages, but not PMNs, was demonstrated. To test whether the effects of TNF-α on the outcome of infection are mediated by macrophages/monocytes, we systemically depleted C57BL/6 mice of monocytes by pharmacological and genetic approaches. Systemic monocyte depletion substantially increased bacterial dissemination from soft tissues without affecting the number of recruited PMNs or altering the bacterial loads in soft tissues. Enhanced GAS dissemination could be reverted by either i.v. injection of monocytes or s.c. administration of peritoneal macrophages. These experiments demonstrated that recruited macrophages play a key role in defense against the extracellular pathogen GAS by limiting its spread from soft tissues.

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Section: Resultssupporting

confidence: 82%

Recruited Macrophages Control Dissemination of Group A Streptococcus from Infected Soft Tissues

Mishalian

Ordan

Peled³

et al. 2011

The Journal of Immunology

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“…We next examined the expression pattern of TNF-α, a cytokine involved in the augmentation of inflammatory responses to bacterial infection. Indeed, development of GAS-necrotizing fasciitis has been reported as a complication of anti-TNF-α therapy (37). As shown in Figure 7A, GAS strongly induced TNF-α mRNA production in WT macrophages.…”

Section: Figurementioning

confidence: 86%

HIF-1α expression regulates the bactericidal capacity of phagocytes

Peyssonnaux¹,

Datta²,

Cramer³

et al. 2005

J. Clin. Invest.

638

695

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Hypoxia is a characteristic feature of the tissue microenvironment during bacterial infection. Here we report on our use of conditional gene targeting to examine the contribution of hypoxia-inducible factor 1, α subunit (HIF-1α) to myeloid cell innate immune function. HIF-1α was induced by bacterial infection, even under normoxia, and regulated the production of key immune effector molecules, including granule proteases, antimicrobial peptides, nitric oxide, and TNF-α. Mice lacking HIF-1α in their myeloid cell lineage showed decreased bactericidal activity and failed to restrict systemic spread of infection from an initial tissue focus. Conversely, activation of the HIF-1α pathway through deletion of von Hippel-Lindau tumor-suppressor protein or pharmacologic inducers supported myeloid cell production of defense factors and improved bactericidal capacity. HIF-1α control of myeloid cell activity in infected tissues could represent a novel therapeutic target for enhancing host defense.

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“…3, 4 We report herein 5 cases of interstitial granulomatous dermatitis (IGD) occurring in patients receiving 4 different agents with TNF-␣ inhibitory activity.…”

Section: Umor Necrosis Factormentioning

confidence: 99%

Interstitial Granulomatous Dermatitis Associated With the Use of Tumor Necrosis Factor α Inhibitors

Deng¹,

Harvey²,

Sina³

et al. 2006

Arch Dermatol

152

105

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Necrotising fasciitis in a patient receiving infliximab for rheumatoid arthritis

Cited by 79 publications

References 8 publications

Recruited Macrophages Control Dissemination of Group A Streptococcus from Infected Soft Tissues

Recruited Macrophages Control Dissemination of Group A Streptococcus from Infected Soft Tissues

HIF-1α expression regulates the bactericidal capacity of phagocytes

Interstitial Granulomatous Dermatitis Associated With the Use of Tumor Necrosis Factor α Inhibitors

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