The effect of diabetes mellitus on chemotactic and bactericidal activity of human polymorphonuclear leukocytes

Naghibi, Morteza; Smith, Raymond P.; Baltch, Aldona L.; Gates, Sherman A.; Wu, David H.; Hammer, Mark C.; Michelsen, Phyllis B.

doi:10.1016/s0168-8227(87)80030-x

Cited by 75 publications

(41 citation statements)

References 23 publications

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“…In addition to these alterations, NOD mice show an impaired recruitment of professional phagocytes in response to local inflammation (Bouma et al 2005), which is associated with a deficient production of local chemokines and an increased secretion of IL-10. Moreover, it has been shown that neutrophils derived from diabetic patients have decreased bactericidal activity, resulting in further delays in pathogen destruction and, therefore, delays in the tissue repair and wound healing processes (Delamaire et al 1997;Naghibi et al 1987). …”

Section: Resultsmentioning

confidence: 99%

Rescuing of deficient killing and phagocytic activities of macrophages derived from non-obese diabetic mice by treatment with geldanamycin or heat shock: potential clinical implications

Vega

Charles

Alexander

2011

Cell Stress and Chaperones

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Diabetes mellitus type 1 (DMT1) is an autoimmune disease characterized by the destruction of insulinproducing cells in the pancreas. Diabetic patients are more susceptible to recurrent and uncontrolled infections, with worse prognoses than in healthy individuals. Macrophages (Mfs) derived from DMT1 individuals have compromised mounting of inflammatory and immune responses. The mechanisms responsible for these alterations remain unknown. It has been shown that the presence of extra-and intracellular heat shock proteins (hsp) positively modulates immune cell function. Using naive Mfs derived from nonobese diabetic (NOD) mice, a well-established mouse model for DMT1, we demonstrate that heat shock (HS) as well as treatment with geldanamycin (GA), significantly improves diabetic Mf activation, resulting in increased phagocytosis and killing of bacteria. Induction of HS did not affect the aberrant NOD-Mf cytokine profile, which is characterized by elevated IL-10 levels and normal tumor necrosis factor alpha. Our observations were consistent at pre-diabetic (normal random blood glucose) and diabetic (random blood glucose greater than 250 mg/dl) stages, suggesting that HS and GA treatment may compensate for intrinsic genetic alterations present in diabetic cells regardless of the stage of the disease. The mechanisms associated to this phenomenon are unknown, but they may likely be associated with the induction of hsp expression, a common factor between HS and GA treatment. Our results may open a new field for non-classical function of hsp and indicate that hsp expression may be used as a part of therapeutic approaches for the treatment of complications associated with DMT1 as well as other autoimmune diseases.

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Section: Resultsmentioning

confidence: 99%

Rescuing of deficient killing and phagocytic activities of macrophages derived from non-obese diabetic mice by treatment with geldanamycin or heat shock: potential clinical implications

Vega

Charles

Alexander

2011

Cell Stress and Chaperones

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“…As a result, the cutaneous defense response and the skin microbiome are likely to be highly interactive, maintaining a delicate balance between defending against infection and eliciting an excessive inflammatory response. Further, chronic inflammation has been implicated in the pathogenesis of nonhealing diabetic wounds (10)(11)(12)(13). Necrotic tissue and low oxygen tension present in the wound encourage proliferation and colonization of microbes.…”

mentioning

confidence: 99%

Longitudinal shift in diabetic wound microbiota correlates with prolonged skin defense response

Grice

Snitkin

Yockey

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

203

173

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Diabetics frequently suffer from chronic, nonhealing wounds. Although bacterial colonization and/or infection are generally acknowledged to negatively impact wound healing, the precise relationship between the microbial community and impaired wound healing remains unclear. Because the host cutaneous defense response is proposed to play a key role in modulating microbial colonization, we longitudinally examined the diabetic wound microbiome in tandem with host tissue gene expression. By sequencing 16S ribosomal RNA genes, we show that a longitudinal selective shift in wound microbiota coincides with impaired healing in diabetic mice ( Lepr db/db ; db/db). We demonstrate a parallel shift in longitudinal gene expression that occurs in a cluster of genes related to the immune response. Further, we establish a correlation between relative abundance of Staphylococcus spp. and the expression of cutaneous defense response genes. Our data demonstrate that integrating two types of global datasets lends a better understanding to the dynamics governing host–microbe interactions.

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“…35 Depressed immune system functioning also puts diabetics at increased risk for wound infection. [36][37][38] Diabetic foot ulcers are a major risk factor for limb amputation, 39 because osteomyelitis of the underlying bone is not uncommon. 40 For healing and avoidance of recurrence, patients with sensory neuropathy must wear protective footwear at all times to prevent repeated trauma.…”

Section: Arterial Ulcersmentioning

confidence: 99%

Treating the chronic wound: A practical approach to the care of nonhealing wounds and wound care dressings

Fonder

Lazarus

Cowan

et al. 2008

Journal of the American Academy of Dermatology

554

439

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The effect of diabetes mellitus on chemotactic and bactericidal activity of human polymorphonuclear leukocytes

Cited by 75 publications

References 23 publications

Rescuing of deficient killing and phagocytic activities of macrophages derived from non-obese diabetic mice by treatment with geldanamycin or heat shock: potential clinical implications

Rescuing of deficient killing and phagocytic activities of macrophages derived from non-obese diabetic mice by treatment with geldanamycin or heat shock: potential clinical implications

Longitudinal shift in diabetic wound microbiota correlates with prolonged skin defense response

Treating the chronic wound: A practical approach to the care of nonhealing wounds and wound care dressings

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