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High cytokine levels in perforated acute otitis media exudates containing live bacteria

Artikel i vetenskaplig tidskrift
Författare Susann Skovbjerg
Kristian Roos
Forough Nowrouzian
Magnus Lindh
Stig Holm
Ingegerd Adlerberth
Sigvard Olofsson
Agnes E Wold
Publicerad i Clinical microbiology and infection
Volym 16
Nummer/häfte 9
Sidor 1382–1388
ISSN 1469-0691
Publiceringsår 2010
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 1382–1388
Språk en
Länkar dx.doi.org/10.1111/j.1469-0691.2009...
Ämnesord otitis media, cytokines, prostaglandin
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

Acute otitis media (AOM) is an inflammatory response to microbes in the middle ear, sometimes associated with rupture of the tympanic membrane. Human leukocytes produce different patterns of inflammatory mediators in vitro when stimulated with Gram-positive and Gram-negative bacteria, respectively. Here, we investigated the cytokine and prostaglandin E(2) (PGE(2)) responses in middle ear fluids (MEFs) from children with spontaneous perforated AOM and related the levels to the presence of pathogens detected by culture (live) or PCR (live or dead). Furthermore, in vivo cytokine pattern was compared with that induced in leukocytes stimulated by dead bacteria in vitro. MEFs with culturable pathogenic bacteria contained more IL-1beta (median 110 vs <7.5 ng/ml), TNF (6.3 vs <2.5 ng/ml), IL-8 (410 vs 38 ng/ml), and IL-10 (0.48 vs <0.30 ng/ml), than culture negative fluids, irrespective of PCR findings. IL-6 and PGE(2) were equally abundant (69-110 ng/ml) in effusions with live, dead or undetectable bacteria. Cytokine levels were unrelated to bacterial species and to the presence or absence of virus. Similar levels of TNF and IL-6 as found in the MEFs were obtained by in vitro stimulation of leukocytes, while 11x more IL-1beta and 3.5x more IL-8 was produced in vivo, and 22x more IL-10 was produced in vitro. A vigorous production of pro-inflammatory cytokines accompany AOM with membrane rupture regardless of causative agent, but the production seems to cease rapidly once the bacteria are killed and fragmented. IL-6 and PGE(2), however, remain after bacterial disintegration and may play a role in the resolution phase.

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