Chronic Middle Ear Effusions: Immunochemical and Bacteriological Investigations

Liu, Yea S.; Lim, David J.; Lang, R.; Birck, Herbert G.

doi:10.1001/archotol.1975.00780340010003

Cited by 177 publications

(34 citation statements)

References 35 publications

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“…Previous data indicate that 77% of middle ear effusions from patients with OM exhibit bacterial cells by Gram staining; however, only 52% or less are culture positive (19). The use of formalin-killed NTHI was developed over 15 years ago to simulate this clinical window, i.e., when the acute inflammatory phase has resolved and bacterial pathogens have been killed by either antibiotics or host immune mechanisms, and it is a widely used method of inducing sterile OM (26).…”

Section: Discussionmentioning

confidence: 99%

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Formalin-KilledHaemophilus influenzaeor Its LipooligosaccharidehtrBandrfaDMutants

et al. 2001

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To define the role of nontypeable Haemophilus influenzae (NTHI) lipooligosaccharide (LOS) in the inductionConsiderable evidence indicates that endotoxin or its subcomponent lipopolysaccharide (LPS) or lipooligosaccharide (LOS), each an integral component of the outer membrane of gram-negative bacteria, is refractile and present in a large percentage of middle ear effusions from children with otitis media (OM) (10,14). Endotoxin is a potent stimulant of proinflammatory reactions of the host's innate immune response (22). The inflammatory cytokines are thought to be of central importance in the pathogenesis and regulation of proliferation, chemotaxis, and activation of inflammatory cells during the course of middle ear infections (21, 29). A previous report from our laboratory indicates that there is a significant correlation between endotoxin, tumor necrosis factor alpha (TNF-␣), and interleukin 1␤ (IL-1␤) concentrations in middle ear effusions from children with OM (35). Recent experimental studies, moreover, demonstrate that formalin-killed nontypeable Haemophilus influenzae (NTHI) stimulates the release of IL-1␤, IL-6, IL-8, and TNF-␣ from the middle ear mucosa in the guinea pig OM model (30). It has been proposed that the initial interaction of endotoxin with middle ear epithelium leads to the production and release of inflammatory cytokines in the middle ear (2,5,8). This is followed by recruitment of neutrophils, eruption of a cytokine-mediated inflammatory cascade, and neutrophil activation, resulting in the release of inflammatory molecules which participate directly in middle ear inflammation (27,37). To date, reports on the effects of NTHI LOS on induction of cytokine gene expression by human cells have focused primarily on stimulation of monocytes (34) and bronchial and tracheal epithelial cells (7,16,24). The effects of NTHI LOS on cytokine and chemokine gene expression by cultured human middle ear epithelial (HMEE) cells have never been reported.Major advances have also been made recently in identifying the molecular mechanisms underlying LPS or endotoxin recognition and signaling for LPS-induced cell activation. It is believed that membrane-bound CD14 (mCD14), a glycosyl phosphatidylinositol-anchored protein expressed on myeloid cells, binds to LPS and initiates its signaling (33). Toll-like receptors (TLRs) have been identified as the signaling molecules and may act as transmembrane coreceptors with CD14 in LPS activation of different cell populations (15). The potential role of NTHI LOS in the activation of HMEE cells via these pathways has also not been explored.It is now possible to define the role of NTHI LOS in the pathogenesis of OM by using mutants with various LOS gene disruptions as tools. A recent study from our laboratory indicates that disruption of the NTHI htrB and rfaD LOS genes does not impact the ability of NTHI to colonize the nasopharynx; however, it induces marked differences in the abilities of

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Section: Discussionmentioning

confidence: 99%

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Formalin-KilledHaemophilus influenzaeor Its LipooligosaccharidehtrBandrfaDMutants

et al. 2001

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“…120 Á 123 The effusion level of IgM in some patients with chronic otitis media was markedly elevated. 120 The mucoid type of effusions contained a high level of IgG, IgA 121 and IgE. 124 Comparison of the immunoglobulin levels measured in effusions and in sera showed that, in many cases, the effusion level of secretory IgA 122 and IgE 125 was significantly higher than the corresponding serum level, and this was the evidence of local overproduction of immunoglobulins in the middle ear.…”

Section: Immunoglobulins In Chronic Omementioning

confidence: 99%

The Relation between Tympanostomy Tube Otorrhea and Types of Immune Cells in Middle Ear Effusion in Children with Otitis Media with Effusion

Lim¹,

Hyun²,

Kim³

et al. 2018

Korean J Otorhinolaryngol-Head Neck Surg

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Inflammation in the middle ear mucosa, which can be provoked by different primary factors such as bacterial and viral infection, local allergic reactions and reflux, is the crucial event in the pathogenesis of otitis media with effusion (OME). Unresolved acute inflammatory responses or defective immunoregulation of middle inflammation can promote chronic inflammatory processes and stimulate the chronic condition of OME. Cytokines are the central molecular regulators of middle ear inflammation and can switch the acute phase of inflammation in the chronic stage and induce molecular Á /pathological processes leading to the histopathological changes accompanying OME. In this review we present cytokines identified in otitis media, immunoregulatory [interleukin (IL)-2, IL-10, transforming growth factorb]) and allergy associated (IL-4, IL-5, granulocyte Á / macrophage colony-stimulating factor), as crucial molecular regulators, responsible for chronic inflammation in the middle ear and the chronic condition of OME.

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“…Otitis media indicates an inflammatory condition in volving the middle car [1], in a certain percentage of which the ear has a concurrent infection [2,3]. The fact that the Eustachian tube in young children is wider appears to en courage spread of infection to the middle car [4], Such in fection is more often bilateral, although accompanying earache may be limited only to one side or be entirely ab sent.…”

Section: Introductionmentioning

confidence: 99%

“…Children with SOM appear to have an increased in cidence of allergic conditions, frequently affecting the up per respiratory area [13], which involve secretion from mast cells [20], These cells contain numerous secretory granules, each of which stores many biologically active molecules [21] which include histamine and kinins, as well as a variety of cytokines such as interleukin-1 (IL-1) and tu mor necrosis factor (TNF) which are both inflammatory and vasoactive [22], In addition, mast cells synthesize de novo prostaglandin D2 (PGD2), leukotriene C2 (LTC4) which are vasodilatory, and a number of chemotactic fac tors for other inflammatory cells. These mediators could lead to congestion of the upper respiratory area and the Eustachian tube, as well as the middle ear, thus also pro viding an attractive medium for bacterial growth [2,3], In turn, inflammatory cells recruited to this area could set up a delayed inflammatory reaction which chronically de scribes this condition [23].…”

mentioning

confidence: 99%

Treatment of Secretory Otitis media with Local Instillation of Hydroxyzine

Theoharides

Manolidis²,

Vliagoftis³

et al. 1994

Int Arch Allergy Immunol

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The study is a preliminary single-blind, placebo- and prednisolone-controlled investigation of the treatment of 156 children with otitis media with effusion (secretory otitis media, SOM), ranging from 2 to 12 years. The protocol involved tympanotomy and placement of a ventilation tube (grommet), through which control or drug solutions were introduced. Other parameters and coexisting symptoms which could contribute to SOM were also examined. Patients were divided into 3 groups as follows: group A: control (normal saline, 2 ml); group B: prednisolone (25 mg in 2 ml); group C: hydroxyzine pamoate (10^––⁵ M in 2 ml). The results indicate that in those children treated with hydroxyzine, the rate of relapse was significantly reduced and so was the amount of histamine present in middle ear effusions. The effectiveness of hydroxyzine is discussed in the context of the pathophysiology of SOM, especially with respect to mast cells and their activation by allergic and nonallergic means.

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Chronic Middle Ear Effusions: Immunochemical and Bacteriological Investigations

Cited by 177 publications

References 35 publications

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Formalin-KilledHaemophilus influenzaeor Its LipooligosaccharidehtrBandrfaDMutants

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Formalin-KilledHaemophilus influenzaeor Its LipooligosaccharidehtrBandrfaDMutants

The Relation between Tympanostomy Tube Otorrhea and Types of Immune Cells in Middle Ear Effusion in Children with Otitis Media with Effusion

Treatment of Secretory Otitis media with Local Instillation of Hydroxyzine

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