Z Gastroenterol 2018; 56(01): E2-E89
DOI: 10.1055/s-0037-1612865
Poster Visit Session V Viral Hepatitis and Immunology – Saturday, January 27, 2018, 11:00am – 11:45am, Foyer area East Wing
Georg Thieme Verlag KG Stuttgart · New York

Mucosal invariant T (MAIT) cells are depleted from blood in advanced cirrhosis and accumulate in the peritoneal cavity during bacterial peritonitis

O Akinhanmi
1   Jena University Hospital, Dpt. of Internal Medicine IV, Jena
,
S Stengel
1   Jena University Hospital, Dpt. of Internal Medicine IV, Jena
,
N Köse
1   Jena University Hospital, Dpt. of Internal Medicine IV, Jena
,
A Stallmach
1   Jena University Hospital, Dpt. of Internal Medicine IV, Jena
2   Jena University Hospital, Center for Sepsis Control and Care (CSCC), Jena
,
M Bauer
3   Jena University Hospital, Department of Anesthesiology and Intensive Care, Jena
2   Jena University Hospital, Center for Sepsis Control and Care (CSCC), Jena
,
T Bruns
1   Jena University Hospital, Dpt. of Internal Medicine IV, Jena
2   Jena University Hospital, Center for Sepsis Control and Care (CSCC), Jena
› Author Affiliations
Further Information

Publication History

Publication Date:
03 January 2018 (online)

 

Background:

Mucosal invariant T (MAIT) cells are a subset of the fast-acting unconventional T cells, which play essential roles in mucosal immunity against pathogens. Patients hospitalized for advanced cirrhosis have a poor short-term prognosis especially when they encounter bacterial infections, such a spontaneous bacterial peritonitis (SBP), as a result of impaired immune responses.

Aims:

To investigate the phenotype, function, and clinical relevance of MAIT cells in the peritoneal cavity during complications of cirrhosis.

Methods:

Peripheral blood and ascitic fluid from patients with decompensated cirrhosis and healthy controls were analyzed using flow cytometry. Vα7.2 CD161 CD3 MAIT cells were quantified and markers of activation (CD69), tissue homing (Integrin αE, CCR7), immune exhaustion (PD-1), and intracellular cytokines were assessed.

Results:

Circulating MAIT cell frequencies were significantly lower in patients with decompensated cirrhosis (median 0.7%) compared to controls (median 4.3%; P < 0.0001) without significant correlation with classical liver disease scores. In the absence of SBP, the proportion of MAIT cells among T cells was higher in the peritoneal cavity than in blood (1.0% vs. 0.6%; P = 0.02), and peritoneal MAIT cells had a tissue homing phenotype (CD103 CCR7-). Peripheral blood and peritoneal MAIT cells expressed more often CD69 than conventional T cells (13.9% vs. 0.4%; P = 0.001, 12.5% vs. 1.7%; P = 0.01 respectively) but did not differ in their expression of PD-1.

During SBP, peritoneal MAIT cell frequency (1.2% vs. 2.7%; P = 0.02) and MAIT cell ascites-blood-ratio (1.4 vs. 5.2; P = 0.007) was increased at the day of diagnosis but normalized after 2 days of antibiotic treatment (5.2 vs. 2.0; P = 0.06). As compared to conventional T cells, PMA/ionomycin-stimulated MAIT cells were potent producers of IL-17 and TNF, especially when isolated from ascitic fluid as compared to whole blood.

Conclusion:

These results suggest that activated MAIT cells deplete from blood in advanced cirrhosis and accumulate in the peritoneal cavity in the early phase of SBP.