Escherichia coli‐induced immune paralysis is not exacerbated during chronic filarial infection

Sepsis initially starts with a systemic inflammatory response ( SIRS phase) and is followed by a compensatory anti‐inflammatory response syndrome ( CARS ) that causes impaired adaptive T‐cell immunity, immune paralysis and an increased susceptibility to secondary infections. In contrast, parasitic filariae release thousands of microfilariae into the peripheral blood without triggering inflammation, as they induce regulatory, anti‐inflammatory host responses. Hence, we investigated the impact of chronic filarial infection on adaptive T‐cell responses during the SIRS and CARS phases of a systemic bacterial infection and analysed the development of T‐cell paralysis following a subsequent adenovirus challenge in BALB /c mice. Chronic filarial infection impaired adenovirus‐specific CD 8 + T‐cell cytotoxicity and interferon‐ γ responses in the absence of a bacterial challenge and led to higher numbers of splenic CTLA ‐4 +   CD 4 + T cells, whereas splenic T‐cell expression of CD 69 and CD 62 ligand, serum cytokine levels and regulatory T‐cell frequencies were comparable to naive controls. Irrespective of filarial infection, the SIRS phase dominated 6–24 hr after intravenous Escherichia coli challenge with increased T‐cell activation and pro‐inflammatory cytokine production, whereas the CARS phase occurred 6 days post E. coli challenge and correlated with high levels of transforming growth factor‐ β and increased CD 62 ligand T‐cell expression. Escherichia coli ‐induced impairment of adenovirus‐specific CD 8 + T‐cell cytotoxicity and interferon‐ γ production was not additionally impaired by chronic filarial infection. This suggests that filarial immunoregulation does not exacerbate E. coli ‐induced T‐cell paralysis..

Medienart:

Artikel

Erscheinungsjahr:

2015

Erschienen:

2015

Enthalten in:

Zur Gesamtaufnahme - volume:145

Enthalten in:

Immunology - 145(2015), 1, Seite 150-160

Sprache:

Englisch

Beteiligte Personen:

Buerfent, Benedikt C [VerfasserIn]
Gondorf, Fabian [Sonstige Person]
Wohlleber, Dirk [Sonstige Person]
Schumak, Beatrix [Sonstige Person]
Hoerauf, Achim [Sonstige Person]
Hübner, Marc P [Sonstige Person]

Links:

Volltext
onlinelibrary.wiley.com
www.ncbi.nlm.nih.gov
search.proquest.com

BKL:

44.45

Themen:

CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - pathology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - pathology
Compensatory anti‐inflammatory response syndrome
Escherichia coli - immunology
Escherichia coli Infections - genetics
Escherichia coli Infections - immunology
Escherichia coli Infections - pathology
Filariasis - genetics
Filariasis - immunology
Filariasis - pathology
Filarioidea - immunology
Helminth
Immune paralysis
Interferon-gamma - genetics
Interferon-gamma - immunology
Sepsis
Systemic Inflammatory Response Syndrome - genetics
Systemic Inflammatory Response Syndrome - immunology
Systemic Inflammatory Response Syndrome - pathology
T‐cell cytotoxicity
Transforming Growth Factor beta - genetics
Transforming Growth Factor beta - immunology

RVK:

RVK Klassifikation

doi:

10.1111/imm.12435

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

OLC1964045754