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Updated: Jan 24, 2026
Modeling Persistent Pseudomonas aeruginosa Infection in Wounded Zebrafish Larvae
Published on: June 13, 2025
Lung infection caused by Pseudomonas aeruginosa in a CD26/DPP4 deficient F344 rat model
Background:
Pseudomonas aeruginosa (PA) is the most important opportunistic pathogen in causing nosocomial infections and, furthermore, poses a permanent threat for severe chronic infections in patients with cystic fibrosis or COPD. The transmembrane protein CD26 with dipeptidyl peptidase-4 (DPP4) activity shows an increased expression in inflamed tissue. We tested whether CD26/DPP4 deficiency leads to reduced inflammation and decreased structural damage when infected with PA.
Methods:
CD26/DPP4+ and CD26/DPP4- rats were instilled intratracheally with NaCl (controls) or with PA. Six hours later, bacterial distribution was detected with the in vivo imaging system 200 (IVIS). Lungs were then processed for molecular biology, light and electron microscopy and analyzed qualitatively, quantitatively and stereologically. Bacterial numbers were determined in homogenized lungs.
Results:
Compared to saline treated controls, in both infected groups (1) the acinar airspace was significantly increased, (2) the volume density of the alveolar epithelium was significantly decreased, (3) the septal thickness was significantly reduced, (4) more than 40% of the alveolar epithelial surface was damaged, and up to 36% of the epithelial surface was covered with edema. In infected CD26- rats, the increase in lung weight was significantly less pronounced, the portion of edematous alveolar airspace was significantly lower and the part of edema interspersed with PA was decreased significantly.
Conclusions:
CD26/DPP4 deficiency resulted in reduced pulmonary edema under sublethal PA infection, implicating a role for CD26 in infection progression. The partly pronounced structural damage may mask further possible influences of CD26 on the inflammatory response.
Insights
CD26/DPP4 deficiency reduced lung edema and bacterial spread in rats infected with Pseudomonas aeruginosa (PA). This suggests CD26 plays a role in PA infection progression and lung damage.
Area of Science:
- Pulmonary medicine
- Infectious diseases
- Immunology
Background:
- Pseudomonas aeruginosa (PA) is a critical opportunistic pathogen causing hospital-acquired infections and chronic lung diseases like cystic fibrosis and COPD.
- CD26, a transmembrane protein with dipeptidyl peptidase-4 (DPP4) activity, is upregulated in inflamed tissues.
- The role of CD26/DPP4 in PA infection and associated lung pathology remains unclear.
Purpose of the Study:
- To investigate the impact of CD26/DPP4 deficiency on pulmonary inflammation and structural damage during Pseudomonas aeruginosa infection.
- To determine if lacking CD26/DPP4 influences the host's response to PA, specifically regarding edema and tissue integrity.
Main Methods:
- Rats genetically deficient in CD26/DPP4 (CD26/DPP4-) and wild-type controls (CD26/DPP4+) were intratracheally instilled with PA or saline.
- Bacterial distribution was assessed using in vivo imaging.
- Lung tissues were analyzed using molecular biology, light and electron microscopy, and stereology for bacterial load, edema, and structural changes.
Main Results:
- PA infection led to increased airspace, decreased alveolar epithelium volume, reduced septal thickness, and significant epithelial damage and edema in both groups.
- CD26/DPP4-deficient rats exhibited significantly less lung weight increase and a lower proportion of edematous alveolar airspace compared to infected controls.
- The extent of edema interspersed with PA was also significantly decreased in CD26/DPP4-deficient rats.
Conclusions:
- CD26/DPP4 deficiency confers protection against pulmonary edema during sublethal PA infection.
- These findings highlight a potential role for CD26/DPP4 in the progression of PA infections.
- Further research is needed to fully elucidate the influence of CD26 on the inflammatory response and structural damage in the context of PA infection.
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