Nonsteroidal Anti‐Inflammatory Drugs and Corticosteroids

Clark‐Price, Stuart C.

doi:10.1002/9781118999196.ch5

Cited by 7 publications

(4 citation statements)

References 144 publications

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“…Additionally, there may be other chemotherapeutic regimes that can more effectively modulate disease tolerance. For instance, corticosteroids dampen inflammation by acting on molecules further upstream of those targeted by NSAIDs (Clark‐Price, 2014). While there is some evidence that pre‐infection baseline corticosterone levels and subsequent conjunctivitis negatively correlate in house finches (Adelman et al, 2015), this relationship varies by sex (Love et al, 2016), suggesting a complex role for the hormone in MG pathology.…”

Section: Discussionmentioning

confidence: 99%

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Ruden

Adelman

2022

J Exp Zool Pt A

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Individual animals vary greatly in their responses to infection, either killing off the invading pathogen (resistance) or minimizing the per‐pathogen costs of infection on host fitness (tolerance). Though we understand little about the physiological drivers of tolerance in wild animals, phenotypically, it manifests as milder clinical signs of disease. Here, we use a well‐described disease system, finch mycoplasmosis, to evaluate the role of inflammation in disease tolerance. House finches (Haemorhous mexicanus) infected with the bacterial pathogen Mycoplasma gallisepticum (MG) develop conjunctival pathology that satisfies the cardinal signs of inflammation. We report on a captive trial performed in 2016 and replicated in 2018 that tested whether chemotherapeutics, specifically nonsteroidal anti‐inflammatory drugs (NSAIDs), can reduce lesion severity, thus pushing individuals toward more tolerant phenotypes. Though birds treated with NSAIDs in the first trial developed milder pathology per unit pathogen load, we found no effect of treatment in the second trial, perhaps due to natural variation in baseline tolerance within the source population across years. Second‐trial control birds developed markedly milder pathology than first‐year controls, suggesting that the effect of trial swamped the effect of treatment in this study. Moving forward, using birds from a population in which the disease is absent or only recently emerged—and so tolerance has not yet been selected for—may better elucidate the role of pro‐inflammatory mediators in disease tolerance.

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Section: Discussionmentioning

confidence: 99%

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Ruden

Adelman

2022

J Exp Zool Pt A

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“…Concurrent anti-inflammatory and prostaglandin analogs —NSAIDs and corticosteroids inhibit the formation of prostaglandin from arachidonic acid via the inhibition of cyclooxygenase or phospholipase A, respectively [ 63 ]; consequently, these drugs could theoretically inhibit the indirect action of prostaglandin analogs, that is, synthesis of endogenous prostaglandins that further act on prostaglandin F2α (FP) receptors. In dogs, concurrent administration of latanoprost and flurbiprofen [ 60 ], or latanoprost and prednisolone acetate [ 64 ], resulted in a notable reduction of the ocular hypotensive effect relative to latanoprost therapy alone (20.4% and 56%, respectively) [ 60 , 64 ].…”

Section: Anti-inflammatory Therapy For Eyes Predisposed or Affected B...mentioning

confidence: 99%

Role of Inflammation in Canine Primary Glaucoma

Sebbag,

Pe’er

2023

Animals

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Primary glaucoma is a painful, progressive, and blinding disease reported in many canine breeds, characterized by intraocular pressure (IOP) elevation in the absence of antecedent intraocular disease. Clinical observations of dogs with primary glaucoma suggest that many affected eyes develop concurrent intraocular inflammation in addition to elevated IOP. In this work, we summarize the current knowledge that relates inflammation to primary glaucoma in dogs, reviewing studies focused on genetics, physiology, histopathology, bioanalysis of ocular fluids, therapeutics, and clinical outcomes of glaucomatous patients. Through disruption of the blood–aqueous and blood–retinal barriers, pigment dispersion, and biochemical changes to the aqueous humor and tear film, the pathogenesis of canine primary glaucoma appears to involve inflammatory changes to various extents and with various consequences from the front to the back of the eye. Among others, inflammation further impacts IOP by reducing aqueous humor outflow at the level of the iridocorneal angle and accelerates vision loss by promoting neuronal degeneration. As such, the vicious cycle of ocular inflammation and IOP elevation might warrant the use of anti-inflammatory medications as a core component of the treatment regime for dogs with primary glaucoma, either therapeutically (i.e., actively glaucomatous eye) or prophylactically in the yet unaffected contralateral eye.

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“…Despite decades of research, corticosteroids and nonsteroidal anti-inflammatory drugs (AIDs) remain the primary pharmacological weapons available to control inflammation . Regrettably, these drugs have important side effects, particularly when used long-term. , Similar side effects have been observed for synthetic and clinically used compounds like indomethacin (IMC) and local anesthetics , such as lidocaine (LCN), procaine (PCN), and mepivacaine (MCN).…”

Section: Introductionmentioning

confidence: 99%

Modulation of Phospholipase A₂ Membrane Activity by Anti-inflammatory Drugs

Jaramillo-Granada,

Li,

Flores Villarreal

et al. 2024

Langmuir

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The phospholipase A 2 (PLA 2 ) superfamily consists of lipolytic enzymes that hydrolyze specific cell membrane phospholipids and have long been considered a central hub of biosynthetic pathways, where their lipid metabolites exert a variety of physiological roles. A misregulated PLA 2 activity is associated with mainly inflammatory-derived pathologies and thus has shown relevant therapeutic potential. Many natural and synthetic anti-inflammatory drugs (AIDs) have been proposed as direct modulators of PLA 2 activity. However, despite the specific chemical properties that these drugs share in common, little is known about the indirect modulation able to finely tune membrane structural changes at the precise lipid-binding site. Here, we use a novel experimental strategy based on differential scanning calorimetry to systematically study the structural properties of lipid membrane systems during PLA 2 cleavage and under the influence of several AIDs. For a better understanding of the AIDs-membrane interaction, we present a comprehensive and comparative set of molecular dynamics (MD) simulations. Our thermodynamic results clearly demonstrate that PLA 2 cleavage is hindered by those AIDs that significantly reduce the lipid membrane cooperativity, while the rest of the AIDs oppositely tend to catalyze PLA 2 activity to different extents. On the other hand, our MD simulations support experimental results by providing atomistic details on the binding, insertion, and dynamics of each AID on a pure lipid system; the drug efficacy to impact membrane cooperativity is related to the lipid order perturbation. This work suggests a membrane-based mechanism of action for diverse AIDs against PLA 2 activity and provides relevant clues that must be considered in its modulation.

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Nonsteroidal Anti‐Inflammatory Drugs and Corticosteroids

Cited by 7 publications

References 144 publications

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Role of Inflammation in Canine Primary Glaucoma

Modulation of Phospholipase A₂ Membrane Activity by Anti-inflammatory Drugs

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Nonsteroidal Anti‐Inflammatory Drugs and Corticosteroids

Cited by 7 publications

References 144 publications

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Modulating disease phenotype in a songbird: A role for inflammation in disease tolerance?

Role of Inflammation in Canine Primary Glaucoma

Modulation of Phospholipase A2 Membrane Activity by Anti-inflammatory Drugs

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Product

Resources

About

Modulation of Phospholipase A₂ Membrane Activity by Anti-inflammatory Drugs