Abstract
Granuloma is a medical term for a ball-like collection of immune cells that attempts to remove foreign substances from a host organism. This response is a special type of inflammatory reaction common to a wide variety of diseases. Granulomas are an organised collection of macrophages, whose formation involves the stimulation of macrophages as well as T-Cells. Fault tolerance in swarm robotic systems is essential to the continued operation of swarm robotic systems. Under certain conditions, a failing robot can have a detrimental effect on the overall swarm behaviour, causing stagnation in the swarm and affecting its ability to undertake its task. Our study is concerned specifically with modelling the trafficking of macrophages and T-cells in the development of granuloma formation, and using that as a basis to create a self-healing swarm robotic system, in the context of power system failure.
I. INTRODUCTION
Robustness, self-organisation and adaptation are some of the key properties that have been a source of inspiration for research in swarm robotics. Robustness is a fundamental characteristic of biological systems. As reported in [5], numerous articles have been published on how robustness is involved in various biological processes and on mechanisms that give rise to robustness in living systems [2], [7]. In addition to robustness, other biological properties that have inspired research in swarm robotics are self-organisation and adaptation. Selforganisation is widespread in biological systems, including cells, organisms, and groups that possesses a large number of subunits. These subunits lack either the communicational abilities or the computational abilities, or both, that are needed to implement centralised control [3]. The main contribution of this paper is to demonstrate how modelling the development of granuloma formation can provide useful insight into the understanding of their properties leading to the instantiation of these properties to swarm robots aggregation tasks.
II. GRANULOMA FORMATION
Adams [1] defined granuloma as : ‘a compact (organised) collection of mature mononuclear phagocytes (macrophages and/or epitheliod cells) which may or may not accompanied by accessory features such as necrosis of the infiltration of other inflammatory leukocytes’ From this definition, a simplified version of this terminology is also provided by [1] as an organised collection of macrophages. [1] further explained that granulomas evolve conceptually in three stages. First, is the development of an infiltrate of young mononuclear phagocytes, followed by the maturation and aggregation of these cells (phagocytes) into a mature granuloma, and finally the further maturation of mature granuloma into epithelioid granuloma. Sneller identifies some of the cells involved in granuloma formation [6]. The cells’ interactions start when they are exposed to an antigen. Within seconds, or minutes, of the exposure to the antigen, pre-stored tumor necrosis factor (TNF) released by mast cells recruits neutrophils, which in turn signal to, and circulate, monocytes: this leads to the granulomatous inflammation. Interferon-gamma produced by local natural killer (NK) and T cells further activates resident tissues’ histiocytes and dendritic cells. These, in turn, release a large amount of chemokines and TNF that alter the local microcirculatory environment and facilitate cellular trafficking into tissues. Following the accumulation and activation of macrophages, the inflammatory lesion (region that has suffered damage) begins to take on a granulomatous form. With the arrival of antigen-specific T cells, the lesion transforms into a mature granuloma where activation of macrophages by interferon-gamma and tumor necrosis factor (TNF) results in inhibition (slowing or prevention) of microbial growth. Eventually, the granuloma becomes encapsulated by a fibrotic rim and the center becomes necrotic (death). These tissue reactions function to protect the host by promoting microbial containment (under control) and reducing the nutrient supply to the pathogen


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