Antibiotics, inflammation and its resolution: An overview

Parnham, Michael J.

doi:10.1007/3-7643-7310-5_2

Cited by 4 publications

(4 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Macrolide antibiotics may modulate cytokine expression by human neutrophils, and their ability to increase or decrease cytokines appears to be dependent on the presence or absence of bacteria (49). It has been proposed that macrolides will initially stimulate nonactivated leukocytes but suppress cytokine production in the presence of inflammatory priming (16,43). We have shown that CAM decreases IL-8 secretion in vitro over the first 6 h of exposure in association with a decrease in pERK but increases proinflammatory cytokine release and pERK after 6 h of exposure.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Shinkai¹,

Foster²,

Rubin³

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

141

View full text Add to dashboard Cite

Macrolide antibiotics decrease proinflammatory cytokine production in airway cells from subjects with chronic airway inflammation. However, in subjects with chronic obstructive pulmonary disease, short-term azithromycin (AZM) therapy causes a transient early increase in the blood neutrophil oxidative burst followed by a decrease in inflammatory markers with longer administration. We studied the effects of clarithromycin (CAM) and AZM on proinflammatory cytokine production from normal human bronchial epithelial (NHBE) cells. CAM decreased IL-8 over the first 6 h and then significantly increased interleukin (IL)-8 at 12-72 h after exposure (P < 0.0001). AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). PD-98059, an inhibitor of MAP kinase/ERK kinase, inhibited CAM-induced IL-8 (P < 0.0001) and GM-CSF (P < 0.01) release. The p38 MAP kinase inhibitor SB-203580 increased CAM-induced IL-8 release (P < 0.001), and the c-jun NH2-terminal kinase inhibitor SP-600125 had no effect on IL-8. At 120 min and 6 h, CAM increased phospho-ERK1/2 (pERK) but not phospho-p38 or phospho-JNK. Over the first 90 min, CAM at 10 microg/ml inhibited pERK and then increased pERK in parallel with measured IL-8 secretion. After daily CAM exposure for 5 days, both IL-8 and pERK returned to baseline. The p38 MAP kinase inhibitor, SB-203580 increased ERK phosphorylation and IL-8 secretion. These results suggest that macrolide antibiotics can differentially modulate proinflammatory cytokine secretion in NHBE cells, in part through ERK.

show abstract

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that macrolides initially stimulate nonactivated leukocytes but suppress cytokine production in the presence of inflammatory priming (16,43).…”

mentioning

confidence: 99%

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Shinkai¹,

Foster²,

Rubin³

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

141

View full text Add to dashboard Cite

show abstract

“…LPS triggers the synthesis and release of cytokines, NO, and ROS [60] [61]. Thus inhibition of unresolved inflammation, either by antibiotics or specifically anti-inflammatory agents is needed to relieve patients with chronic inflammatory disorders [13].…”

Section: Discussionmentioning

confidence: 99%

“…This is coincided with the fact that the immune system response to a microorganism may be beneficial in infection, and has the potential to be more devastating than direct damage caused by a microbe, but facilitated resolution of the response is needed to limit tissue damage [12] [13]. So that the potential benefits of down regulating immunomodulators entered the limelight, with the understanding that immune hyper-activation for example in sepsis, can have disastrous consequences [11].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection

El-Banna¹,

El-Aziz²,

El-Mahdy³

et al. 2015

JBM

View full text Add to dashboard Cite

There is growing interest in re-evaluation of older antibiotics with the wide spread of pathogen resistance, especially gram negative bacteria, which impair treatment of some infections. In contrast various studies have reported that some antibiotics have efficacy in clearing resistant bacterial infections. On account of that it was interesting to evaluate the efficacy of erythromycin, chloramphenicol and/or tenoxicam in curing and/or relieving wound infection of highly resistant Escherichia coli and investigate the possible mechanisms beyond their antibacterial activity. This was achieved through evaluating highly resistant E. coli strains in vitro using agar dilution and in vivo rat models of E. coli infected wound and acute inflammation by carrageenin, where possible mechanisms were evaluated through measuring immunological mediators and histopathological examination. This study revealed that in vivo, erythromycin alone or in combination with tenoxicam significantly improved the healing of infected skin wounds with E. coli irresspective of resistancy in vitro. In addition to the improvement of immunological mediators involved in inflammatory reaction, oxidative stress and in cytokines expression as response to the bacterial infection in vivo. On the other hand chloramphenicol neither alone nor in combination with tenoxicam, achieved any significant effect. Tenoxicam didn't show antimicrobial activity alone nor in combination with tested antibiotics in vitro, but it has shown synergestic activity in combination with tested antibiotics in vivo. Thus we concluded that immunomodulatory activity of erythromycin through anti-inflammatory and antioxidant effects was the possible mechanisms by which this antibiotic had healed infection with resistant E. coli in vivo, despite its resistancy to this antibiotic in vitro.

show abstract

A review of hot and sweet pepper added in animal nutrition: alternative against the use of antibiotics

Flores-Tejeida

Soto-Zarazúa

Guevara-González

et al. 2018

2018 XIV International Engineering Congress (CONIIN)

View full text Add to dashboard Cite

Antibiotics, inflammation and its resolution: An overview

Cited by 4 publications

References 88 publications

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection

A review of hot and sweet pepper added in animal nutrition: alternative against the use of antibiotics

Contact Info

Product

Resources

About

Antibiotics, inflammation and its resolution: An overview

Cited by 4 publications

References 88 publications

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Macrolide antibiotics modulate ERK phosphorylation and IL-8 and GM-CSF production by human bronchial epithelial cells

Efficacy of Some Antibiotics in Curing Resistant &lt;i&gt;Escherichia coli&lt;/i&gt; Infection

A review of hot and sweet pepper added in animal nutrition: alternative against the use of antibiotics

Contact Info

Product

Resources

About

Efficacy of Some Antibiotics in Curing Resistant <i>Escherichia coli</i> Infection