Chemokines and chemokine receptors in infectious diseases

Mahalingam, Surendran; Karupiah, Gunasegaran

doi:10.1046/j.1440-1711.1999.00858.x

Cited by 100 publications

(76 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cytokine burst is not necessarily linked to macrophage lysis, although the rapid release of IL-1β, as early as 150 minutes, probably reflects release of intracellular stores concomitant with lysis, since induction of IL-1β mRNA is not observed. Transitory production of other cytokines could be a response of various cells to IL-1β (43)(44)(45)(46)(47). The remarkable production of eotaxin and the KC induction in hepatocytes confirm involvement of other cell types and at the same Figure 10 LT induction of FasL and cytotoxicity in FasL-deficient mice.…”

Section: Discussionmentioning

confidence: 89%

Bacillus anthracis lethal toxin induces TNF-α–independent hypoxia-mediated toxicity in mice

Moayeri¹,

Haines²,

Young³

et al. 2003

J. Clin. Invest.

View full text Add to dashboard Cite

Bacillus anthracis lethal toxin (LT) is the major virulence factor of anthrax and reproduces most of the laboratory manifestations of the disease in animals. We studied LT toxicity in BALB/cJ and C57BL/6J mice. BALB/cJ mice became terminally ill earlier and with higher frequency than C57BL/6J mice. Timed histopathological analysis identified bone marrow, spleen, and liver as major affected organs in both mouse strains. LT induced extensive hypoxia. Crisis was due to extensive liver necrosis accompanied by pleural edema. There was no evidence of disseminated intravascular coagulation or renal dysfunction. Instead, analyses revealed hepatic dysfunction, hypoalbuminemia, and vascular/oxygenation insufficiency. Of 50 cytokines analyzed, BALB/cJ mice showed rapid but transitory increases in specific factors including KC, MCP-1/JE, IL-6, MIP-2, G-CSF, GM-CSF, eotaxin, FasL, and IL-1β. No changes in TNF-α occurred. The C57BL/6J mice did not mount a similar cytokine response. These factors were not induced in vitro by LT treatment of toxin-sensitive macrophages. The evidence presented shows that LT kills mice through a TNF-α–independent, FasL-independent, noninflammatory mechanism that involves hypoxic tissue injury but does not require macrophage sensitivity to toxin

show abstract

Section: Discussionmentioning

confidence: 89%

Bacillus anthracis lethal toxin induces TNF-α–independent hypoxia-mediated toxicity in mice

Moayeri¹,

Haines²,

Young³

et al. 2003

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…IL-8 synthesis and release is triggered in response to various stimuli including LPS, TNF-α, and IL-1β [113] . Important cell sources of IL-8 in the gut are macrophages, endothelial cells, intestinal epithelial cells, and fibroblasts [114] .…”

Section: Il-8mentioning

confidence: 99%

“…Important cell sources of IL-8 in the gut are macrophages, endothelial cells, intestinal epithelial cells, and fibroblasts [114] . IL-8 exerts its effects by binding to chemokine receptors CXCR1 and CXCR2 that signal through phospholipase c and PI3-kinase, respectively [113] . Some actions mediated by IL-8 are attraction of neutrophils and basophils to the site of inflammation, neutrophil activation and migration into tissues and production of acute phase proteins [114] .…”

Section: Il-8mentioning

confidence: 99%

Necrotizing enterocolitis: A multifactorial disease with no cure

Schnabl

Aerde²,

Thomson³

et al. 2008

WJG

160

120

View full text Add to dashboard Cite

INTRODUCTIONNecrotizing enterocolitis (NEC) is an inflammatory bowel disease of neonates and remains one of the most common gastrointestinal emergencies in newborn infants [1] . Onset of NEC is often within the first three months of life and neonates who are of extremely low birth weight (< 1000 g) and under 28 wk gestation are the most susceptible [2] . Full term neonates account for 10% of all NEC cases while premature infants account for 90% [3] . With an incidence rate of 1%-5% for all newborns admitted to the NICU [1] , a prevalence of 7%-14% of very low birth weight infants (VLBW, 500-1500 g) [4] and a mortality rate approaching 20%-50% [5] , NEC continues to represent a significant clinical problem. In Canada, the incidence rate is 1.8 per 100 live births with a prevalence of 7% of VLBW infants [1] . Advances in obstetric and neonatal care have improved survival rates for smaller, more immature infants, and as more VLBW preterm infants survive the neonatal period, the population at risk for NEC increases [1] .No consistent association between sex, race, and rates of NEC has been identified. However, male VLBW infants and black infants are at greater risk of death [6] . Due to inadequate treatments and no effective preventative strategy, an estimated 20%-40% of babies with NEC require surgery [1] and 10%-30% experience significant morbidity including neurodevelopmental impairment, vision and hearing impairment, failure to thrive, feeding abnormalities, diarrhea, bowel obstruction, and short bowel syndrome [1,2,7] . The case fatality rate with surgical intervention is as high as 50% [1] . NEC is also a financial burden to the health care system with yearly hospital charges reported to be as high as $6.5 million in the US [8] . Thus, NEC continues to be an important health issue for preterm neonates. DIAGNOSIS Clinical signs and symptomsThe onset of NEC can occur suddenly within a few AbstractNecrotizing enterocolitis is an inflammatory bowel disease of neonates with significant morbidity and mortality in preterm infants. Due to the multifactorial nature of the disease and limitations in disease models, early diagnosis remains challenging and the pathogenesis elusive. Although preterm birth, hypoxic-ischemic events, formula feeding, and abnormal bacteria colonization are established risk factors, the role of genetics and vasoactive/inflammatory mediators is unclear. Consequently, treatments do not target the specific underlying disease processes and are symptomatic and surgically invasive. Breast-feeding is the most effective preventative measure. Recent advances in the prevention of necrotizing enterocolitis have focused on bioactive nutrients and trophic factors in human milk. Development of new disease models including the aspect of prematurity that consistently predisposes neonates to the disease with multiple risk factors will improve our understanding of the pathogenesis and lead to discovery of innovative therapeutics.

show abstract

“…Chemokines mediate chemotaxis and leukocyte activation. They also regulate leukocyte extravasation from the blood and/or lymph vessel luminal surface to the tissue space, the site of inflammation (Mahalingam and Karupiah, 1999). We first evaluated TNF-␣, a chemokine known to induce a local Shwartzman reaction.…”

Section: Skin Ulcers After Il-8 Overexpressionmentioning

confidence: 99%

Interleukin-8 Overexpression Is Present in Pyoderma Gangrenosum Ulcers and Leads to Ulcer Formation in Human Skin Xenografts

Oka

Berking

Nesbit

et al. 2000

Laboratory Investigation

113

View full text Add to dashboard Cite

SUMMARY: ) is a potent chemotactic polypeptide for neutrophils. However, the role of this cytokine during inflammation remains unclear. Skin specimens from patients with pyoderma gangrenosum demonstrated IL-8 overexpression in skin ulcers, which suggests a role for IL-8 in the development of the disease. We therefore constructed a recombinant adenovirus expressing the complementary deoxyribonucleic acid encoding human IL-8 (IL-8/Ad5) that induces a 2000-fold increase in IL-8 expression of infected human fibroblasts in vitro. Human skin engrafted to severe combined immunodeficiency mice and then injected with the recombinant virus demonstrated erythema, an intense perivascular infiltration of neutrophils, and extravasation of erythrocytes after 8 hours. By 12 hours after injection, neutrophils had accumulated beneath the epidermis, which then necrotized, and one or more ulcers that remained for approximately 2 weeks were observed. Clinically and histologically, the ulcers resembled pyoderma gangrenosum. These clinical and experimental findings suggest an etiologic role of IL-8 in the pathogenesis of pyoderma gangrenosum. (Lab Invest 2000, 80:595-604).

show abstract

Chemokines and chemokine receptors in infectious diseases

Cited by 100 publications

References 81 publications

Bacillus anthracis lethal toxin induces TNF-α–independent hypoxia-mediated toxicity in mice

Bacillus anthracis lethal toxin induces TNF-α–independent hypoxia-mediated toxicity in mice

Necrotizing enterocolitis: A multifactorial disease with no cure

Interleukin-8 Overexpression Is Present in Pyoderma Gangrenosum Ulcers and Leads to Ulcer Formation in Human Skin Xenografts

Contact Info

Product

Resources

About