**1. Introduction**

Inflammation is a natural phenomenon for healing that occurs through the body's immune response. The cellular reactions remove the threat that may be in the form of a pathogen, damaged cell, irritant, and other foreign particles. Often, they are self-limiting; however, under certain circumstances, they can cause permanent damages to healthy tissues and eventually to the entire organ system. The phenomenon of inflammation is caused by specific lipid-derived and small molecular weight proteins referred to as eicosanoids and cytokines, respectively. The cellular and systemic level of eicosanoids and cytokines, and the relative presence of pro- vs. anti-inflammatory mediators determines overall inflammatory milieu in an individual. Uncontrolled and chronic inflammation triggers

many common conditions and diseases. Bronchitis, conjunctivitis, chronic obstructive pulmonary disease (COPD), hepatitis, irritable bowel disease (IBD), psoriasis, rheumatoid arthritis (RA), and rhinitis are known to have a critical link with eicosanoids productions that eventually leads inflammation [1–8]. Even though effective pharmaceutical interventions are available to treat as well as manage these complications, adjunct therapies involving dietary management is mostly recommended [9, 10]. Nutraceutical intervention in the management of these inflammatory complications is gaining importance due to convenience, safety, and the low-cost attached in it Investigations have pointed out that n-3 polyunsaturated fatty acids (n-3 PUFA) positively alter inflammatory pathways. Their actions aid in reduced levels of eicosanoids (20 carbon lipid-derived molecules) and other inflammatory biomarkers, such as interleukin-1b (IL-1b), IL-6, and tumor necrosis factor-α (TNF- α) in plasma and urine, by serving as secondary messengers or modifying the transcriptional regulation of particular genes involved in inflammation [11]. In contrast, a high intake of dietary n-6 polyunsaturated fatty acids (n-6 PUFA) is associated with increased synthesis of proinflammatory eicosanoids synthesized from arachidonic acid metabolism, which include leukotrienes, lipoxins, thromboxanes, prostaglandins, and hydroxy fatty acids, and suppresses the synthesis of anti-inflammatory eicosanoids derived from EPA and DHA [12].

The modern (mostly western) diet is a poor source of n-3 PUFA, with an abysmal n-3:n-6 fatty acid ratio of 1:15–20, which is in sharp contrast to that found in the diet followed by our ancestors-1:1 [13, 14]. Both n-3 and n-6 PUFA consumed in the diet compete for the same enzymes and also regulate many transcription factors which impact cellular and tissue metabolism, and, a skewed ratio of n-3:n-6 PUFA result in the altered equilibrium in composition and fluidity of cell membrane as well as the functionality of organs [15, 16]. Evidence is accumulating that these physiological changes have led to interactions between constituents of the diet and genes, culminating in the rise of local and systemic inflammation. It is coupled with the disruption of immune/defense mechanism leading to rheumatoid arthritis, chronic obstructive pulmonary disease, irritable bowel diseases, psoriasis, bronchitis, rhinitis, hepatitis, conjunctivitis, etc.
