Pulmonary and muscle profile in pneumosepsis: A temporal analysis of inflammatory markers

Area of Science:

• Critical Care Medicine
• Immunology
• Pathophysiology

Background:

• Sepsis involves complex inflammatory responses impacting multiple organs.
• Understanding sepsis-induced inflammation, particularly its effects on skeletal muscle, is crucial for critically ill patients.
• Klebsiella pneumoniae (K.p.) is a common cause of hospital-acquired pneumonia and sepsis.

Purpose of the Study:

• To investigate the inflammatory profile in lungs and skeletal muscles during K.p. pneumosepsis within the first 72 hours.
• To assess the impact of K.p. infection on physical capacity and inflammatory markers in mice.
• To determine if early skeletal muscle injury contributes to reduced physical performance in this sepsis model.

Main Methods:

• Male BALB/c mice were inoculated intratracheally with K.p. or PBS, with assessments at 24, 48, and 72 hours.
• Maximum Physical Capacity Test (MPCT) was used to evaluate physical performance.
• Pulmonary inflammation was assessed via bronchoalveolar lavage fluid (BALF) analysis (cell counts, NOx, IL-1β, TNF-α).
• Muscle inflammation and trophism were evaluated using ELISA and Western blotting for TNF-α, IL-6, TGF-β, BDNF, and NF-κB.

Main Results:

• Sepsis groups exhibited increased BALF total cells, blood granulocytes, and decreased MPCT performance.
• Nitric oxide (NOx) levels significantly increased at 72 hours post-infection.
• Early lung inflammation (PS24) showed elevated TNF-α and bacterial load (CFU); muscle showed increased IL-6 and nuclear NF-κB.

Conclusions:

• Early K.p. pneumosepsis leads to significant pulmonary inflammation and reduced physical capacity.
• While early muscle IL-6 and NF-κB elevations occurred, skeletal muscle tissue showed minimal injury.
• Reduced physical performance in this model is likely attributable to lung inflammation rather than direct, early skeletal muscle damage.