Modulatory role of eosinophils in allergic inflammation: new evidence for a rather outdated concept

Bandeira‐Melo, Christianne; Cordeiro, Renato S.B.; Silva, Patrícia M.R.; Martins, Marco A.

doi:10.1590/s0074-02761997000800007

Cited by 3 publications

(4 citation statements)

References 33 publications

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“…This eosinophilia was long lasting and it did not affect the onset of the pleural edema following Ag challenge. We have also previously shown that pleural eosinophilia, induced by local administration of eosinophil attractants such as platelet-activating factor, ECF-A, bacterial LPS, and pleural wash from LPS-treated rats (16 -18), also promotes an attenuation of allergen-induced pleural edema within 4 h. Selective inhibition of eosinophil influx by either immunological or pharmacological means diminished the curtailment of allergic edema, reinforcing the relationship between eosinophilia and down-regulation of allergic edema (16,18).…”

Section: Discussionmentioning

confidence: 76%

“…PGE 2 is one of the eicosanoids produced by eosinophils (30,31), and Buijs et al (15) had noted that parasitic infection increased the biosynthesis of PGE 2 concurrent with eosinophilia. Furthermore, allergic stimulation raised PGE 2 production in pleural cavities that were experiencing a concurrent selective eosinophilia induced by eosinophil chemoattractants (17,18).…”

Section: Discussionmentioning

confidence: 99%

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Cyclooxygenase-2-Derived Prostaglandin E2 and Lipoxin A4 Accelerate Resolution of Allergic Edema inAngiostrongylus costaricensis-Infected Rats: Relationship with Concurrent Eosinophilia

Bandeira‐Melo¹,

Serra²,

Diaz³

et al. 2000

The Journal of Immunology

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126

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In noninfected rats, challenge with allergen following local IgE sensitization induced a pleurisy marked by intense protein exudation that plateaued from 30 min to 4 h after challenge, reducing thereafter. Infection of rats with Angiostrongylus costaricensis induced a 5-fold increase in blood eosinophil numbers by 25 days postinfection, whereas the numbers of eosinophils in the pleural cavity ranged from normal to a weak increase. In infected rats, identically sensitized, challenge with Ag induced a much shorter duration of pleural edema with complete resolution by 4 h, but no change in the early edema response. In parallel, infection increased the number of eosinophils recovered from the pleural cavity at 4 h, but not at 30 min, following allergen challenge. Pretreatment with IL-5 (100 IU/kg, i.v.) also increased eosinophil numbers in blood and, after allergen challenge, shortened the duration of the pleural edema and increased pleural eosinophil numbers. There were increases in the levels of both PGE2 and lipoxin A4 (LXA4) in pleural exudate. Selective cyclooxygenase (COX)-2 inhibitors, NS-398, meloxicam, and SC-236, did not alter pleural eosinophilia, but reversed the curtailment of the edema in either infected or IL-5-pretreated rats. Pretreatment of noninfected animals with the PGE analogue, misoprostol, or two stable LXA4 analogues did not alter the magnitude of pleural exudation response, but clearly shortened its duration. These results indicate that the early resolution of allergic pleural edema observed during A. costaricensis infection coincided with a selective local eosinophilia and seemed to be mediated by COX-2-derived PGE2 and LXA4.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2-Derived Prostaglandin E2 and Lipoxin A4 Accelerate Resolution of Allergic Edema inAngiostrongylus costaricensis-Infected Rats: Relationship with Concurrent Eosinophilia

Bandeira‐Melo¹,

Serra²,

Diaz³

et al. 2000

The Journal of Immunology

Self Cite

126

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“…Recent investigations have established that activated eosinophils can damage normal tissues in the course of chronic inflammatory and allergic diseases25, 26 by releasing various cytotoxic substances such as cationic proteins13, 27–29, leukotriene B4, platelet activating factor, and various cytokines24. McGovern et al 3.…”

Section: Discussionmentioning

confidence: 99%

The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes afterHelicobacter pylori eradication

et al. 2000

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Helicobacter pylori (HP)-infected gastric mucosa displays a conspicuous infiltration of mononuclear cells as well as neutrophils. RANTES is a potent chemoattractant peptide for memory T lymphocytes and eosinophils. RANTES protein concentration and the numbers of RANTES-, CD45RO-, and major basic protein (MBP)-positive cells were therefore evaluated in the gastric mucosa from 51 patients with HP-positive chronic gastritis before and after HP eradication and from 22 HP-negative healthy volunteers. RANTES protein concentration was significantly elevated in HP-positive cases and remained high after HP eradication. The numbers of RANTES-, CD45RO-, and MBP-positive cells were significantly increased in HP-positive cases and were well correlated with RANTES protein levels. All tended to decrease after HP eradication, but did not reach the level of HP-negative cases, even at 24 months after HP eradication. It was concluded that persistent expression and secretion of RANTES were closely related to residual infiltration of memory T lymphocytes and eosinophils, for a prolonged period after HP eradication. This seems to be an important mechanism of prolonged gastric mucosal immune response against HP infection, even after HP eradication, and of persistent mucosal damage and atrophy.

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“…45 In disease states, eosinophils have also been reported to have some role in hypersensitivity reactions. 46,47 However, the absence of mast cells and basophils, the main cells associated with hypersensitivity reactions, indicated the absence of hypersensitivity reactions during the study period with all of the scaffolds used in this studied. Eosinophils were absent in the fibrous tissue surrounding CEM at 21 days, and their V v at 63 days was less than 0.2%.…”

Section: Discussionmentioning

confidence: 79%

Characterization of Tissue Response and in Vivo Degradation of Cholecyst-Derived Extracellular Matrix

Burugapalli

Pandit

2007

Biomacromolecules

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A rat subcutaneous implantation model was used to evaluate the in vivo degradation and tissue response of cholecyst-derived extracellular matrix (CEM). This response was compared to that of glutaraldehyde (GA) cross-linked CEM and porcine heart valve (HV), which are designated as GAxCEM and GAxHV, respectively. Tissue composition, inflammatory cell distribution, and angiogenesis at the implant site were quantified using stereological parameters, thickness (Ta), volume fraction (Vv), surface density (Sv), length density (Lv), and radius of diffusion (Rdiff). CEM was completely infiltrated with host tissue at 21 days and resorbed by 63 days. GAxCEM was also infiltrated with host tissue, while GAxHV matrix was impermeable to host tissue infiltration. Both GAxCEM and GAxHV retained their scaffold integrity until 63 days with no apparent degradation. A fibrous tissue of thickness <52 mum, rich in collagen and vasculature, surrounded all scaffolds, and from 21 to 63 days the fibrous tissue showed maturation with a significant increase in their fibrocyte content. No signs of acute inflammatory response were observed in the study period for any of the scaffolds, while the chronic inflammatory response was predominated with macrophages for all scaffolds except for CEM at 63 days. A higher degree of giant cell formation was observed with GA cross-linked scaffolds. From 21 to 63 days, lymphocytic response decreased for CEM, while it increased significantly for GAxHV. Angiogenesis/neo-vascularization was uniform for CEM (reaching the core), significantly lower for GAxCEM within the implant area as compared to CEM, while restricted to the exterior of GAxHV matrix. In summary, CEM was a fast degrading scaffold that induced a transitional inflammatory response accompanied by gradual resorption and replacement by host connective tissue as compared to the very slow degrading GA cross-linked controls, GAxCEM and GAxHV, which caused a sustained chronic inflammatory response and remained at the site of implantation until the end of the study period of 63 days.

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Modulatory role of eosinophils in allergic inflammation: new evidence for a rather outdated concept

Cited by 3 publications

References 33 publications

Cyclooxygenase-2-Derived Prostaglandin E2 and Lipoxin A4 Accelerate Resolution of Allergic Edema inAngiostrongylus costaricensis-Infected Rats: Relationship with Concurrent Eosinophilia

Cyclooxygenase-2-Derived Prostaglandin E2 and Lipoxin A4 Accelerate Resolution of Allergic Edema inAngiostrongylus costaricensis-Infected Rats: Relationship with Concurrent Eosinophilia

The relationship between persistent secretion of RANTES and residual infiltration of eosinophils and memory T lymphocytes afterHelicobacter pylori eradication

Characterization of Tissue Response and in Vivo Degradation of Cholecyst-Derived Extracellular Matrix

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